FRIESNER  AND  BRAUN  i 


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CEREBELLAR  ABSCESS 


The  First  Scientific  Figures  of  the  Cerebellum,  from 
Reproduced  from  a  copy  kindly  loaned  to 


"HuMANi  Fabrica"  of  Andreas  Vesalius,  1555. 
the  Publisher  by   Dr.  Abraham  Jacobi. 


CEREBELLAR  ABSCESS 

ITS  ETIOLOGY,  PATHOLOGY,  DIAGNOSIS 
AND  TREATMENT 

INCLUDING 
ANATOMY  AND  PHYSIOLOGY  OF  THE  CEREBELLUM 


BY 


ISIDORE  FRIESNER,  m.d. 

ADJUNCT     PROFESSOR     OF      OTOLOGY      AND 

ASSISTANT    AURAL    SURGEON,     MANHATTAN 

EYE.      EAR     AND     THROAT      HOSPITAL     AND 

POST    GRADUATE   MEDICAL  SCHOOL, 

NEW    YORK 


6?      ALFRED  BRAUN,  m.d.,  f  a.c.s. 

ASSISTANT     AURAL    SURGEON,      MANHATTAN 

EYE.    EAR  AND  THROAT  HOSPITAL.  ADJUNCT 

PROFESSOR    OF    LARYNGOLOGY.    NEW     YORK 

POLYCLINIC.     ADJUNCT     OTOLOGIST. 

MT.  SINAI  HOSPITAL 


WITH    lO    FULL    PAGE    PLATES    AND    l6    ILLUSTRATIONS    IN    TEXT 


NEW  YORK 

PAUL  B.  HOEBER 

1916 


Copyright,  1916, 
By  PAUL  B.  HOEBER 


Published  June,  1916 


Printed  in  the  United  States  of  America 


PREFACE 

Ninety-eight  per  cent  of  cerebellar  abscesses  are 
otitic  in  origin,  and  the  diagnosis  and  treatment  of 
this  complication  are,  to-day,  almost  solely  the  prov- 
ince of  the  otological  surgeon. 

Considering  the  recent  advances  made  in  our 
knowledge  of  cerebellar  physiology  and  methods  of 
diagnosis,  and  particularly  of  the  relationship  be- 
tween the  cerebellum  and  the  static  labyrinth,  a  work 
on  cerebellar  abscess  is  not  untimely.  This  relation- 
ship we  have  described  at  length,  trusting  that  it  will 
interest  the  neurologist  as  well  as  the  otologist. 

In  this  book,  we  have  attempted  to  outline  briefly 
the  anatomy  and  physiology  of  the  cerebellum  as  a 
basis  for  that  neurological  knowledge  with  which  the 
surgeon  must  be  equipped  in  order  to  cope  with  the 
problem  of  cerebellar  diagnosis.  We  have  made  no 
attempt  to  state  all  the  opinions  with  regard  to  the 
physiology,  but  have  confined  ourselves  to  those  hy- 
potheses which  seemed  most  plausible  and  which  shed 
most  light  upon  the  subject.  The  etiology,  pathology 
and  symptomatology  have  been  based  chiefly  upon  the 
reports  of  86  cases  which  we  have  been  able  to  collect 
from  the  literature  since  1906.     The  illustrations  are 

9 


3576bi> 


10  PREFACE 

from  original  drawings  and  photographs  made  by  one 
of  us  (Braun). 

We  have  made  no  attempt  to  mention  every  book 
which  has  been  written  on  this  subject,  but  have  re- 
ferred only  to  those  publications  which  were  used  in 
the  preparation  of  this  work. 

We  wish  to  thank  Dr.  T.  Passmore  Berens,  Dr. 
Wendell  C.  Philhps,  Dr.  Arthur  B.  Duel,  Dr.  John 
B.  Rae,  and  many  of  our  colleagues  at  the  Manhat- 
tan Eye,  Ear  and  Throat  Hospital,  for  the  opportuni- 
ties they  have  afforded  us  to  study  their  cases  of  brain 
abscess. 

We  also  wish  to  thank  Mr.  Paul  B.  Hoeber  for 
many  useful  suggestions,  and  for  the  careful  manner 
in  which  he  and  his  staff  have  prepared  this  volume. 
Isidore  Friesner — Alfred  Braun. 

New  York,  May,  1916. 


CONTENTS 

CHAPTER  PAGE 

I.  Anatomy  of  the  Cerebellum 17 

II.   Physiology  of  the  Cerebellum 51 

III.  Etiology  and  Pathology  of  Cerebellar  Abscess      75 

IV.  Symptoms  of  Cerebellar  Abscess       ....     103 
V.   Prognosis  and  Treatment  of  Cerebellar  Abscess  145 

Bibliography 171 

Index 183 


LIST  OF  ILLUSTRATIONS 

The   First   Scientific   Figures   of   the   CerebeUum,   from 
"Humani  Fabrica"  of  Andreas  VesaUus,  1555    .  Frontispiece 

FIGURE  PAGE 

1.  Relations    of    Cerebellum    with    Posterior    Petrosal 

Surface 18 

2.  Cerebellar  Peduncles 20 

'  3.     Cerebellum,  from  Above 22 

4.  Cerebellum,  from  Below 24 

5.  Vertical  Transverse  Section  through  Cerebellum  and 

Medulla 27 

6.  Histological  Structure  of  Cerebellum 28 

7.  Afferent  Cerebellar  Tracts 34 

8.  Efferent  Cerebellar  Tracts 38 

9.  Brachium  Conjunctivum  and  Secondary  Tracts  from 

Red  Nucleus  and  Optic  Thalamus 42 

10.  Spino-Cerebellar  Tracts 44 

11.  Tracts  to  and  from  Deiters'  Nucleus 46 

12.  Cerebellar  Reflex  Arc 57 

13.  Cerebellum,  Lateral  View 66 

14.  Cerebellum,  Posterior  View 68 

15.  Pointing  Test  for  Rotation 115 

16.'   Loss  of  Pointing  Reaction  after  Rotation       .      .      .  117 

17.  Normal  Pointing  Reaction  after  Rotation  to  Left  119 

18.  Pointing  Reaction  with  Caloric  Vestibular  Stimula- 

tion          121 

19.  Pointing  Reaction  at  Elbow  Joint 123 

20.  Pointing  Reaction  at  Wrist  Joint 125 

21.  Operation  for  Cerebellar  Abscess :     Radical  Mastoid 

Operation  Done;  Sinus  Being  Uncovered   .            .  151 

22.  Operation  for  Cerebellar  Abscess:     Sinus  and  Cere- 

bellar Dura  Exposed 153 

23.  Operation  for  Cerebellar  Abscess :     Labyrinthectomy  155 

24.  Operation  for  Cerebellar  Abscess:     Cerebellum  Un- 

covered from  Behind 163 


CHAPTER  I 

ANATOMY    OF   THE    CEREBELLUM 


CHAPTER  I 

ANATOMY    OF    THE    CEREBELLUM 

THE  cerebellum  is  situated  in  the  posterior 
fossa  of  the  skull.  It  occupies  most  of  that 
part  of  the  cranial  cavity  which  lies  below 
the  tentorium  cerebelli.  The  tentorium  is  a  hori- 
zontal process  of  the  dura,  attached  posteriorly  to 
the  inner  surface  of  the  occipital  bone  at  the  level 
of  the  torcular  Herophili  and  the  horizontal  portions 
of  the  lateral  sinuses,  and  laterally  to  the  postero- 
superior  margins  of  the  petrous  pyramids.  Its  ante- 
rior margin  is  crescentic  in  shape  and  free,  and  forms 
the  posterior  boundary  of  an  opening  for  the  passage 
of  the  mid-brain.  It  separates  the  middle  from  the 
posterior  fossa  of  the  skull.  The  occipital  lobes  of 
the  cerebrum  rest  on  its  upper  surface ;  the  cerebellum 
is  in  contact  with  its  lower  surface. 

The  under  surface  of  the  cerebellum  lies  upon  that 
portion  of  the  occipital  bone  below  the  groove  for  the 
lateral  sinus.  Its  middle  portion  lies  above  the  mid- 
brain, pons  and  medulla.  Laterally  it  is  in  relation 
with  the  posterior  surface  of  the  petrous  pyramids. 
Here  it  is  in  close  proximity  to  the  internal  ear.   The 

dura  covering  this  portion  of  the  cerebellum  is  in 

17 


IS 


CEREBELLAR  ABSCESS 


contact   M'ith    the   inner   table   limiting   the  mastoid 
antrum  and  cells. 

Between  the  layers  of  this  portion  of  the  dura  runs 


lAM     5E 


Fig.   1. — Relations  of  Cerebellum  with  Posterior  Petrosal 

Surface. 


lAM,  Internal  auditory  meatus. 
SE3  Saccus  endolymphaticus. 
LS,  Lateral  sinus. 
BV,  Biventral  lobe. 


the  sigmoid  sinus  (Fig.  1).  The  latter  crosses 
obliquely  over  the  lateral  margin  and  anterior  part 
of  the  under  surface  of  the  cerebellum.    About  three- 


ANATOMY  OF  CEREBELLUM         19 

quarters  of  an  inch  to  one  inch  in  front  of  the  middle 
portion  of  the  sinus,  the  cerebellar  dura  is  in  contact 
with  the  internal  auditory  meatus.  JNIidway  between 
the  sinus  and  the  internal  auditory  meatus  the  dura  is 
split  into  two  layers  which  enclose  the  saccus  endo- 
lymphaticus. 

The  middle  portion  of  the  under  surface  of  the 
cerebellum  lies  above  the  posterior  surfaces  of  the 
mid-brain,  pons  and  medulla,  and  with  these  struc- 
tures forms  a  tent-shaped  cavity  known  as  the  fourth 
ventricle.  This  is  continuous  above  with  the  aqueduct 
of  Sylvius  and  below  with  the  central  canal  of  the 
spinal  cord. 

The  recess  on  either  side  of  the  pons,  between  it 
and  the  under  surface  of  the  cerebellum,  is  known  as 
the  cerebello-pontine  angle.  In  this  angle  are  situ- 
ated the  roots  of  the  fifth,  sixth,  seventh,  eighth,  ninth 
and  tenth  cranial  nerves. 

The  cerebellum  is  shaped  somewhat  like  a  complete 
clam  shell,  the  hinge  of  the  clam  shell  lying  anteriorly, 
the  edge  laterally  and  posteriorly,  and  the  flattened 
surfaces  above  and  below.  It  is  divided  into  a  median 
lobe  or  vermis,  to  either  side  of  which  is  joined  a 
lateral  lobe  or  hemisphere.  The  vermis  alone  is  pres- 
ent in  the  lower  vertebrates.  The  lateral  lobes  appear 
in  the  higher  forms  of  vertebrates  and  attain  their 
maximum  development  in  man. 

The  upper  surface  of  the  cerebellum  is  slightly 


20 


CEREBELLAR  ABSCESS 


convex,  with  a  low  antero-posterior  ridge  in  the  center, 
corresponding  to  the  upper  vermis.  The  lower  sur- 
face is  divided  by  a  deep  cleft  into  two  lateral  halves. 
At  the  bottom  of  this  cleft  the  lower  vermis  is  seen  as 


Fig.   2. — Cerebellar  Peduncles, 
SP,  Superior  peduncle. 
MP,  ]\liddle  peduncle. 
IP,  Inferior  peduncle. 
4V,  Fourth  ventricle. 

a  well-marked  ridge.  Into  this  cleft  are  received  the 
mid-brain,  pons  and  medulla,  to  which  the  cerebellum 
is  attached  by  means  of  three  pairs  of  stalks  or  pe- 
duncles, the  superior,  middle  and  inferior.  (Fig.  2.) 
All  three  peduncles  are  composed  of  fibers  which 


AXATOIMY  OF  CEREBELLUM         21 

enter  into  or  leave  the  interior  of  the  cerehelhim. 

The  superior  peduncles  are  two  narrow,  flat  bands 
which  emerge  from  the  upper  and  mesial  part  of  the 
hemispheres  and  pass  upward  and  forward,  gradu- 
ally approaching  each  other  as  they  ascend.  They  lie 
at  first  in  the  lateral  walls  of  the  fourth  ventricle  and 
then  in  the  roof.  They  disappear  from  view  under- 
neath the  posterior  corpora  quadrigemina. 

The  middle  peduncles  are  thick  bundles  of  fibers, 
which  emerge  from  the  lateral  aspect  of  the  pons  and 
enter  the  cerebellum  just  external  to  the  superior 
peduncles. 

The  inferior  peduncles  are  continuous  with  the  resti- 
form  bodies  of  the  medulla,  where  they  form  the 
lateral  walls  of  the  lower  part  of  the  fourth  ventricle. 
They  enter  the  cerebellum  between  the  superior  and 
middle  peduncles. 

The  cerebellum  is  divided  into  an  upper  and  a 
lower  half  by  a  deep  horizontal  fissure.  The  upper 
half  is  divided  by  four  sulci  into  five  lobes.  (Fig.  3.) 
The  sulci,  from  before  backward,  are  the  precentral, 
postcentral,  preclival  and  postclival.  These  fissures 
divide  the  upper  surface  of  the  cerebellum  into  lobes 
which  extend  transversely  across  the  entire  organ. 
The  lobes  on  the  upper  surface  of  the  vermis  are  as 
follows:  In  front  of  the  precentral  fissure  is  the 
lingula;  between  the  pre-  and  postcentral  fissures  is 
the  lobus  centralis;  between  the  ])ostcentral  and  pre- 


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ANATOMY  OF  CEREBELLUM         23 

clival  fissures  is  the  culmen;  between  the  pre-  and 
postclival  fissures  is  the  clivus ;  and  between  the  post- 
clival  and  great  horizontal  fissures  is  the  folium 
cacuminis. 

Every  lobe  of  the  vermis  is  continuous  laterally 
w^th  a  lobe  in  each  hemisphere.  Thus  on  either  side 
of  the  lingula  are  the  frenuia;  on  either  side  of  the 
lobus  centralis  are  the  alee  lobi  centralis;  on  either  side 
of  the  culmen  are  the  anterior  crescentic  lobes;  on 
either  side  of  the  clivus  are  the  posterior  crescentic 
lobes,  and  on  either  side  of  the  folium  cacuminis  are 
the  postero-superior  lobes. 

The  sulci  on  the  inferior  surface  of  the  cerebellum 
from  behind  forward  are,  the  post-pyramidal,  pre- 
pyramidal  and  post-nodular.  (Fig.  4.)  The  lobes  on 
the  under  surface  of  the  vermis  are  as  follows:  Be- 
tween the  great  horizontal  and  the  post-pyramidal  fis- 
sures is  the  tuber  valvul^e ;  between  the  post-  and  pre- 
pyramidal  fissures  is  the  pyramid;  between  the  pre- 
pyramidal  and  post-nodular  fissures  is  the  uvula,  and 
in  front  of  the  post-nodular  fissure  is  the  nodulus. 
The  lobes  on  the  under  surface  of  the  hemispheres  are 
as  follows :  On  either  side  of  the  tuber  valvulas  are  the 
postero-inferior  lobes;  on  either  side  of  the  pyramid 
are  the  biventral  lobes ;  on  either  side  of  the  uvula  are 
the  tonsils,  and  on  either  side  of  the  nodule  are  the 
flocculi.  The  biventral  lobe  is  in  relation  with  the  pos- 
terior surface  of  the  petrous  pyramid.     The  internal 


24 


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25 


26  CEREBELLAR  ABSCESS 

auditory  meatus  lies  against  its  anterior  surface.  The 
descending  jjart  of  the  lateral  sinus  passes  across  its 
posterior  portion. 

Between  the  deep  fissures,  which  divide  the  sur- 
face into  lobes,  there  are  shallower  clefts,  which  divide 
the  lobes  into  lobules,  so  that  the  surface  of  the  cere- 
bellum has  a  laminated  appearance.  The  laminae  run 
transversely. 

On  section  the  cerebellum  is  seen  to  consist  of  gray 
cortex  and  central  white  matter.  In  the  white  matter 
are  masses  of  gray  substance  called  the  central  nuclei. 
(Fig.  5.)  In  man  there  are  four  of  these  in  each  half 
of  the  organ,  viz. : 

1.  Nucleus  Tecti  (nucleus  fastigii  or  nucleus  of 
the  roof.) 

2.  Nucleus  Dentatus. 

3.  Nucleus  Emboliformis. 

4.  Nucleus  Globosus. 

The  vestibular  nuclei  are  often  described  with  the 
cerebellar  nuclei.  The  latter  are  para-cerebellar. 
They  are  the  nucleus  of  Bechterew,  the  nucleus  of 
Deiters  and  the  nucleus  triangularis.  The  nucleus 
emboliformis  and  the  nucleus  globosus  are  considered 
by  Kohnstamm  to  be  upward  prolongations  of  Bech- 
terew's  nucleus. 

The  nuclei  tecti  are  rounded  collections  of  gray 
matter  situated  in  the  white  substance  of  the  vermis. 
They  lie  just  above  the  roof  of  the  fourth  ventricle, 


ANATOMY  OF  CEREBELLUM 


27 


close  to  the  median  line,  and  separated  from  each 
other  hy  a  thin  septum  of  white  matter.     They  con- 


FiG.  5. — Vertical  Transverse  Section  through  Cerebellum 
AND  ]\Iedulla. 

DN,  Dentate  nucleus. 
NT,  Nucleus  tecti. 
NE,  Nucleus  emboliformis. 
NG,  Nucleus  globosus. 
4V,  Fourth  ventricle. 
O,  Medullary  olive. 


sist  of  multipolar  nerve  cells  whose  axons  leave 
the  cerebellum  through  its  peduncles.  It  is  around 
these  cells  that  the  axons  of  the  Purkinje  cells  termi- 
nate. 


Fig.  6. 


28 


Fig.  6. — Histological  Structure  of  Cerebellum. 
ML,  Molecular  layer. 
PL,  Layer  of  Purkinje  cells. 
GL,  Granular  layer. 
W,  White  matter. 
DN,  Dentate  nucleus. 

P,  Purkinje  cell  surrounded  b}^  network  from  basket  cell. 
B,  Basket  cell. 
G,  Granule  cell. 
D,  Cells  in  dentate  nucleus. 
GF,  Climbing  fiber  or  "fibre  grimpante." 
MF,  Mossy  fiber. 


29 


30  CEREBELLAR  ABSCESS 

The  nuclei  dentati  are  the  largest  of  the  cerebellar 
nuclei.  They  are  situated  near  the  center  of  each 
hemisphere.  On  section  they  appear  as  wavy  capsules 
with  an  opening  situated  mesially.  This  opening  is 
called  the  hilus.  In  structure  the  nuclei  dentati  are 
similar  to  the  nuclei  tecti. 

The  nucleus  emboliformis  lies  just  mesial  to  the 
hilus  of  the  dentate  nucleus,  and  between  the  nucleus 
emboliformis  and  the  median  line  is  the  nucleus  glo- 
bosus. 

The  nucleus  of  Deiters  bears  a  close  relationship 
both  physiologically  and  anatomically  to  the  cere- 
bellar nuclei.  It  is  situated  in  the  dorsal  portion  of 
the  medulla  and  pons,  between  the  restiform  body  and 
descending  root  of  the  fifth  nerve.  Although,  accord- 
ing to  Kohnstamm,  it  receives  no  fibers  directly  from 
the  vestibular  nerve,  yet  it  receives  the  vestibular 
stimuli  indirectly  through  the  triangular  nucleus.  It 
receives  fibers  from  and  sends  fibers  to  the  central 
cerebellar  nuclei.  It  sends  fibers  through  the  poste- 
rior longitudinal  fasciculus  to  the  mid-brain,  and 
through  the  Deiterso-spinal  tract  to  the  anterior  horn 
cells  of  the  cord.  The  latter  tract  constitutes  one  of 
the  important  pathways  between  the  cerebellum  and 
spinal  cord. 

The  histology  of  the  cortex  of  the  cerebellum  is 
based  upon  that  of  a  single  lamella,  since  the  structure 
of  the  cortex  is  everywhere  the  same.     Each  lamella 


ANATOMY  OF  CEREBELLUM         31 

is  divided  from  the  surface  to  the  interior  into  four 
layers  (Fig.  6). 

1.  Molecular  layer. 

2'.  Layer  of  Purkinje  cells. 

3.  Granular  layer. 

4.  White  substance. 

The  outer  or  molecular  layer  consists  of  the  den- 
dritic processes  of  the  Purkinje  cells,  the  terminal 
arborizations  of  the  centripetal  cerebellar  fibers,  neu- 
roglia and  two  classes  of  nerve  cells,  viz, :  Small  star- 
shaped  cells  which  lie  superficially,  and  large  star- 
shaped  cells  (called  basket  cells)  which  lie  in  the 
deeper  portions  of  this  layer.  From  the  body  of  each 
large  cell  an  axis-cylinder  is  given  off.  This  axon,  in 
its  course,  sends  out  numerous  collaterals,  which  form 
basket-like  networks  about  the  bodies  of  the  Purkinje 
cells.  The  axon  itself  terminates  in  a  similar  man- 
ner. 

The  Purkinje  cells  lie  between  the  molecular  and 
granular  layers.  They  are  large  pear-shaped  cells 
whose  axons  pass  down  into  the  white  matter  and 
end  in  the  central  nuclei  of  the  cerebellum.  Their 
dendritic  processes  pass  outward  into  the  molecular 
layer  like  the  branches  of  a  tree.  The  branches  spread 
in  the  sagittal  plane,  i.  e.,  at  right  angles  to  the  direc- 
tion of  the  lobules  and  sulci.  These  dendritic  proc- 
esses are  joined  together  by  the  axis-cylinder  proc- 
esses of  the  cells  in  the  granular  layer.     The  Pur- 


32  CEREBELLAR  ABSCESS 

kinje  cells  are  thus  joined  together  in  two  ways,  viz.: 
By  the  granule  cells  and  by  the  basket  cells. 

The  granular  layer  is  composed  almost  entirely  of 
small  round  cells,  which  send  axons  into  the  molecular 
layer.  Here  the  axon  divides  into  two  branches  which 
run  in  opposite  directions  to  each  other,  and  at  right 
angles  to  the  axis-cylinder,  so  that  the  three  form  a 
letter  T.  The  branches  run  in  a  coronal  plane,  i.  e., 
parallel  to  the  cerebellar  sulci,  and  pass  across  the 
dendritic  processes  of  the  Purkinje  cells  very  much 
like  telegraph  wires  across  the  arms  of  telegi-aph  poles. 
Thus  an  impulse  from  the  periphery,  originating  in  a 
few  cells,  is  transmitted  to  a  large  number  of  the  Pur- 
kinje cells. 

The  white  substance  of  the  cerebellum  is  composed 
of  three  classes  of  fibers.  These  fibers  are  grouped  in 
accordance  with  the  direction  of  the  impulses  which 
they  convey  into,  (a)  association,  (b)  centripetal,  (c) 
centrifugal  fibers. 

The  association  fibers  join  one  lobe  or  lobule  with 
another,  or  one  hemisphere  with  the  other. 

The  centripetal  fibers  enter  the  cerebellum  through 
the  peduncles  and  terminate  in  the  cortex  and  central 
nuclei.  Those  which  end  in  the  cortex  are  of  two 
types,  the  so-called  mossy  fibers  and  the  climbing 
fibers,  or  "fibres  grimpantes."  The  mossy  fibers  have 
club-shaped  extremities  and  terminate  about  the 
ffranule   cells.    The   climbing  fibers   end   about   the 


ANATOMY  OF  CEREBELLUM         33 

arborizations  of  the  Purkinje  cells.  Centripetal  im- 
pulses are  therefore  transmitted  to  the  Purkinje  cells 
in  two  ways:  Directly,  by  the  climbing  fibers  and 
indirectly,  by  the  mossy  fibers  through  the  granule 
cells. 

The  centrifugal  fibers  from  the  cortex  consist  en- 
tirely of  the  axis.-cylinder  processes  of  the  Purkinje 
cells.  These  all  end  in  the  central  nuclei,  as  was 
proven  by  Edinger.  In  numerous  experiments  he 
destroyed  the  cerebellar  cortex  by  means  of  formalin 
solution  and  found,  from  the  degeneration  thus 
caused,  that  all  fibers  emanating  from  the  cortex  en- 
tered the  central  nuclei,  where  they  stopped.  From 
the  cells  of  the  central  nuclei  centrifugal  fibers  pass 
out  of  the  cerebellum  through  the  peduncles. 

As  has  been  mentioned  above,  the  cerebellum  is  con- 
nected with  the  other  portions  of  the  central  nervous 
system  by  its  peduncles.  In  the  latter,  fiber-tracts 
pass  to  and  from  the  cerebellum.  The  tracts  which 
pass  to  the  cerebellum,  i.  e.,  the  centripetal  tracts,  are 
as  follows:     (Fig.  7.) 

1.  Flechsig's  tract  from  the  spinal  cord  through  the 
inferior  peduncle  to  the  cortex  of  the  vermis. 

2.  Gowers'  tract  from  the  spinal  cord  through  the 
superior  peduncle  to  the  cortex  of  the  vermis. 

3.  A  tract  of  fibers  from  the  nuclei  of  the  posterior 
columns  of  the  cord  through  the  inferior  peduncle  to 
the  cerebellar  cortex. 


Fig.  7. 


34 


Fig.   7. — Afferent  Cerebellar  Tracts. 
C,  Motor  area  of  cerebral  cortex. 
CH,  Cerebellar  hemisphere. 
V,  Vermis. 
M,  Medulla. 
S,  Skin. 
MU,  Muscle. 

CP,  Motor  tract  from  cerebral  cortex  to  pontine  nuclei. 
PN,  Pontine  nucleus. 
PC,  Middle  peduncle  containing  fibers  from  pontine  nuclei 

to  opposite  cerebellar  cortex. 
FT,  Flechsig's  tract. 
GT,  Gowers'  tract. 
TPC,  Posterior  columns  of  cord. 
NBG,  Nuclei  of  Burdach  and  Goll. 
TPN,   Tract   from  nuclei  of   posterior  columns   of  cord  to 

cerebellum. 
N,  Nucleus  of  lateral  tract. 

TLC,  Tract  from  nucleus  of  lateral  column  to  cerebellum. 
O,  Lower  olive. 
OCT,  Olivo-cerebellar  tract. 
VN,  Vestibular  nerve. 
DN,  Deiters'  nucleus. 

DC,  Fibers  from  Deiters'  nucleus  to  cerebellar  hemisphere. 
DV,  Fibers  from  Deiters'  nucleus  to  vermis. 
4V,  Fourth  ventricle. 


35 


36  CEREBELLAR  ABSCESS 

4.  A  tract  from  the  nucleus  of  the  lateral  columns 
in  the  medulla  through  the  inferior  peduncle  to  the 
cerebellar  cortex. 

5.  Olivo-cerebellar  fibers. 

6.  Tracts  from  Deiters'  nucleus  to  the  cerebellar 
cortex  and  central  nuclei. 

7.  Tracts  from  the  motor  cerebral  cortex  through 
the  middle  peduncle  to  the  opposite  cerebellar  hemi- 
sphere. 

The  tracts  which  pass  from  the  cerebellum,  i.  e., 
the  centrifugal  tracts,  are  as  follows:     (Fig.  8.) 

1.  The  tractus  uncinatus  from  the  nucleus  tecti  to 
Deiters'  nucleus  of  the  opposite  side.  From  here  a 
secondary  tract — the  Deiterso-spinal  tract — passes 
down  in  the  anterior  column  of  the  cord  and  ends 
about  the  anterior  horn  cells. 

2.  A  tract  from  the  dentate  nucleus  to  Deiters' 
nucleus. 

3.  Tracts  from  the  central  nuclei  of  the  cerebel- 
lum to  the  nuclei  of  the  posterior  columns  of  the 
cord. 

4.  Tracts  from  the  central  nuclei  of  the  cerebellum 
to  the  nuclei  of  the  lateral  column. 

5.  The  brachium  conjunctivum  and  accessory 
brachium  from  the  dentate  nucleus  and  nucleus  tecti 
through  the  superior  peduncle  to  the  opposite  red 
nucleus  and  optic  thalamus.  From  the  red  nucleus 
a    secondary    tract — the    rubrospinal    tract — passes 


ANATOMY  OF  CEREBELLUM         37 

down  in  the  opposite  lateral  column  of  the  cord  and 
terminates  about  the  anterior  horn  cells. 

6.  The  ventral  cerebello-thalamic  bundle,  from  the 
dentate  nucleus  to  the  opposite  corpora  quadrigemina 
and  optic  thalamus. 

Flechsig's  tract  (direct  cerebellar  tract;  dorsal 
spino-cerebellar  tract)  begins  in  the  lower  lumbar  re- 
gion of  the  cord.  It  arises  from  a  group  of  cells 
(Clarke's  column)  which  is  situated  at  the  base  of 
the  posterior  horn.  The  fibers  of  this  tract  are  col- 
lected into  a  bundle  which  is  situated  at  the  posterior 
part  of  the  margin  of  the  lateral  column  of  the  cord, 
behind  Gowers'  tract.  At  the  upper  end  of  the  cord 
it  lies  next  to  the  substantia  gelatinosa,  i.  e.,  the  head 
of  the  posterior  cornu.  As  it  passes  into  the  medulla 
it  is  separated  from  this  by  the  spinal  root  of  the  fifth 
nerve  and  then  enters  the  corpus  restiforme  or  inferior 
peduncle.  It  passes  through  the  peduncle  to  the 
cerebellum  where  its  fibers  are  distributed  to  the  cells 
in  the  cortex  of  the  upper  worm  of  both  sides. 

Gowers' tract  (ventral  spino-cerebellar  tract)  takes 
its  origin  in  a  column  of  cells  situated  in  the  lateral 
part  of  the  base  of  the  anterior  horn  and  central  gray 
substance.  The  tract  begins  in  the  lower  lumbar  re- 
gion. It  is  situated  at  the  anterior  portion  of  the 
marffin  of  the  lateral  column  of  the  cord  in  front  of 
Flechsig's  tract.  At  the  upper  end  of  the  cord  it  sepa- 
rates from  Flechsig's  tract,  passing  ventrally  to  the 


Fig.  8. 


38 


Fig.  8. — Efferent  Cerebellar  Tracts. 

C,  Cerebral  cortex. 
MB,  Mid-brain. 

CH,  Cerebellar  hemisphere. 

M,  Medulla. 

SC,  Spinal  cord. 

E,  Ocular  muscle. 

'SIV,  Muscles  of  trunk  and  extremities. 

OT,  Optic  thalamus. 

RN,  Red  nucleus. 

3,  Oculo-motor  nuclei. 

NT,  Nucleus  tecti. 

D,  Dentate  nucleus. 
DN,  Deiters'  nucleus. 
4V,  Fourth  ventricle. 

A,  Fibers  from  cortex  of  cerebellum  to  central  nuclei. 

BC,  Brachium  conjunctivum. 

RC,  Fibers  from  red  nucleus  to  cerebral  cortex. 

TC,  Fibers  from  optic  thalamus  to  cerebral  cortex. 

RS,  Rubro-spinal  or  Monakow's  tract. 

AB,  Accessory  brachium  conjunctivum. 

VCT,  Ventral  cerebello-thalamic  bundle. 

DD,  Tract  from  dentate  to  Deiters'  nucleus. 

TU,  Tractus  uncinatus. 

DS,  Deiterso-spinal  tract. 

AN,  Anterior  nerve  root. 

PLF,  Posterior  longitudinal  fasciculus. 

X,  Oculo-motor  nerve. 


39 


40  CEREBELLAR  ABSCESS 

spinal  root  of  the  fifth  nerve  and  reaches  the  anterior 
outer  portion  of  the  medulla.  It  passes  between  the 
nucleus  of  the  facial  nerve  and  the  upper  olive  and 
then  along  the  outer  side  of  the  lateral  fillet  to  the  an- 
terior extremity  of  the  pons.  Here  it  winds  around 
the  brachium  conjunctivum,  reaches  its  inner  side, 
and,  turning  back  along  with  the  brachium,  it  enters 
the  cerebellum.  Its  fibers  end  in  the  cortex  of  the 
worm  of  both  sides. 

Fibers  originating  in  the  nuclei  of  the  posterior 
columns  of  the  cord.  i.  e.,  the  nuclei  of  GoU  and  Bur- 
dach,  pass  through  the  inferior  peduncles  to  the  cortex 
of  the  cerebellar  hemispheres.  Some  of  the  fibers  of 
the  columns  of  Goll  and  Burdach  enter  the  cerebellum 
directly,  without  being  interrupted  by  the  nuclei  of 
these  columns. 

A  tract  from  the  nucleus  of  the  lateral  column  in 
the  medulla  passes  through  the  inferior  peduncle  to 
the  cerebellar  cortex. 

From  the  inferior  olive  internal  arcuate  fibers  pass 
through  the  opposite  restiform  body  to  the  cortex  of 
the  cerebellar  hemisphere. 

Fiber  tracts  pass  from  Deiters'  nucleus  to  the  cor- 
tex and  central  nuclei  of  the  cerebellum.  These  are 
in  all  probability  part  of  the  vestibulo-cerebellar 
tracts. 

From  the  cortex  of  the  cerebral  hemisphere  fibers 
pass  through  the  internal  capsule  and  crus  cerebri  and 


AXATOMY  OF  CEREBELLUM         41 

terminate  about  cells  scattered  through  the  anterior 
portion  of  the  pons.  From  these  cells  axons  cross  in 
the  pons  and,  passing  through  the  middle  peduncle, 
end  in  the  cortex  of  the  opposite  hemisphere. 

The  fibers  of  the  tractus  uncinatus  arise  in  the  nu- 
cleus tecti;  they  cross  over  in  the  roof  of  the  fourth 
ventricle  to  the  opposite  cerebellar  hemisphere,  where 
they  pass  into  Deiters'  nucleus. 

A  tract  of  fibers  passes  from  the  dentate  nucleus  to 
Deiters'  nucleus  of  the  same  side.  Fibers  also  pass 
from  the  dentate  nucleus  to  the  nuclei  of  the  posterior 
columns  and  to  the  nucleus  of  the  lateral  column. 

The  fibers  of  the  brachium  conjunctivum  (Fig.  9) 
arise  in  the  dentate  nucleus  of  the  cerebellum  and  cross 
over  through  the  tegmentimi  of  the  pons  to  the  teg- 
mentum of  the  opposite  side  of  the  mid-brain  where 
most  of  them  end  in  the  red  nucleus.  A  few  pass  to 
the  optic  thalamus. 

An  accessory  brachium  conjunctivum  arises  from 
the  nucleus  tecti  and  crosses  to  the  opposite  side  of 
the  vermis  where  the  fibers  form  a  sort  of  hood  cov- 
ering the  brachium.  These  fibers  also  end  in  the 
opposite  red  nucleus  and  optic  thalamus. 

From  the  red  nucleus  and  optic  thalamus  fibers  pass 
up  through  the  internal  capsule  to  the  sensori-motor 
area  of  the  cerebral  cortex.  From  the  red  nucleus  a 
fiber  tract  also  passes  downward  through  the  teg- 
mentum of  the  pons  and  medulla  to  the  opposite  lat- 


Fig.  9. 
42 


Fig.    9. — Brachium    Conjunctivum    and    Secondary    Tracts 
FROM  Red  Nucleus  and  Optic  Thalamus. 
DN,  Dentate  nucleus. 
RN,  Red  nucleus. 
OT,  Optic  thalamus. 
LN,  Lenticular  nucleus. 
CC,  Cerebral  cortex. 
BC,  Brachium  conjunctivum. 
M,  Monakow's  tract  or  rubro-spinal  tract. 
CT,  Tract  from  red  nucleus  and  optic  thala- 
mus to  sensori-motor  area  of  cerebral  cortex. 


43 


44 


CEREBELLAR  ABSCESS 


eral  column  of  the  spinal  cord.  It  passes  down 
through  the  entire  length  of  the  spinal  cord,  lying  in 
front  of  the  crossed  pyramidal  tract  and  gives  off 
collaterals  which  terminate  about  the  anterior  horn 
cells.  This  tract  is  called  the  rubro-spinal  or  Mona- 
kow's  tract.      (Fig.  10.)     In  this  way  each  cerebellar 


Fig.   10. — Spino-Cerebellar  Tracts. 
M,  Monakow's  or  rubro-spinal  tract. 

F,  Flechsig's  tract. 

G,  Gowers'  tract. 

D^  Deiterso-spinal  tract. 

hemisphere  is  connected  with  the  opposite  cerebral 
hemisphere  and  with  the  anterior  horn  cells  of  the 
same  side  of  the  cord. 

The  ventral  cerebello-thalamic  bundle  takes  origin, 
according  to  Probst,  in  the  dentate  nucleus.  The 
fibers  pass  through  Deiters'  nucleus  and  then  as  inner 
arcuate  fibers  they  reach  the  central  portion  of  the 
substantia  reticularis  of  the  pons.  Here  they  cross 
the  median  raphe,  bending  around  into  the  sagittal 


ANATOMY  OF  CEUEBELLUJM         45 

plane  between  the  raphe  and  mesial  fillet.  They  then 
pass  upward  and  terminate  in  the  corpora  quadri- 
gemina  and  the  inner  portion  of  the  optic  thalamus. 

According  to  .Kohnstamm,  the  nucleus  of  Deiters 
does  not  receive  the  fibers  of  the  vestibular  nerve 
directly,  but  receives  the  vestibular  impulses  through 
the  intermediation  of  the  triangular  nucleus.  It  re- 
ceives the  tractus  uncinatus  from  the  nucleus  tecti  and 
probably  some  fibers  from  the  dentate  nucleus.  (Fig. 
11.)  It  sends  out  two  centrifugal  tracts;  one  to  the 
spinal  cord  and  the  other  to  the  posterior  longitudinal 
fasciculus.  The  fibers  which  pass  down  into  the  cord 
are  known  as  the  Deiterso-spinal  tract.  They  pass 
inward  from  Deiters'  nucleus  as  inner  arcuate  fibers 
to  the  raphe,  where  they  bend  downward  forming  a 
bundle  at  the  margin  of  the  anterior  fissure  of  the  cord 
and  the  adjacent  portion  of  its  ventral  border.  Pass- 
ing down  to  the  sacral  portion  of  the  cord  they  give 
off  in  their  course  collaterals  to  the  anterior  horn  cells. 

From  Deiters'  nucleus  arcuate  fibers  pass  to  the 
posterior  longitudinal  fasciculus  of  both  sides.  These 
fibers  end  about  the  cells  of  the  nuclei  of  the  third, 
fourth,  and  sixth  nerves. 


46 


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47 


CHAPTER  II 

PHYSIOLOGY    OF    THE    CEREBELLUM 


CHAPTER  II 

PHYSIOLOGY    OF    THE    CEREBELLUJNI 

DESPITE  the  fact  that  for  many  years  both 
the  structure  and  the  function  of  the  cere- 
bellum have  been  the  subject  of  a  great 
deal  of  valuable  research,  there  is  still  much  con- 
cerning the  physiology  of  this  organ  that  is  un- 
known. Of  the  experimental  methods  emploj^ed  for 
the  study  of  cerebellar  function,  three  stand  out  prom- 
inenth\  The  first  is  the  destruction  or  removal  of 
certain  parts  of  or  all  of  the  organ  and  section  of  its 
afferent  or  efferent  tracts;  the  second  is  the  stimula- 
tion, by  means  of  the  electric  current,  of  the  cerebellar 
cortex  and  the  central  nuclei;  and  the  third  is  the 
freezing  of  portions  of  the  cerebellar  cortex  in  man. 
The  great  difficulty  encountered  by  most  of  those 
who  experimented  with  the  first  two  methods,  lay  in 
the  fact  that  a  multitude  of  centers  and  fiber  path- 
waj^s  were  thus  destroyed  or  stimulated  at  one  time. 
]Moreover,  the  proximity  of  extraneous  centers  and 
nerve  pathways  to  the  field  of  operation  rendered 
injury  to  or  stimulation  of  these  almost  unavoidable, 
so  that  the  phenomena  following  such  procedures 
could  not  be  classified  or  interpreted.    After  removal 

51 


52  CEREBELLAR  ABSCESS 

of  parts  of  the  cerebellum  it  was  impossible  to  dif- 
ferentiate between  phenomena  that  resulted  from  de- 
struction and  those  which  resulted  from  irritation. 
Nor  was  it  possible  to  determine  which  reactions  were 
compensatory  and  which  were  due  to  irritation  or 
destruction  of  neighboring  parts. 

The  result  of  this  confusion  was  that,  although 
many  experimenters  observed  sunilar  phenomena  fol- 
lowing destruction  of  parts  of  the  cerebellum,  the  in- 
terpretations of  these  phenomena  varied  and  there  was 
no  unanimity  of  opinion  regarding  the  functions 
ascribed  to  this  organ. 

According  to  Lewandowsky,  the  phenomena  fol- 
lowing removal  of  half  the  cerebellum  in  the  dog 
group  themselves  into  two  periods.  The  first  is  the 
period  of  forced  movements  (Zwangsbewegungen)  ; 
the  second  is  the  period  of  incoordination.  The  forced 
movements  consist  chiefly  of  a  curving  of  the  body,  a 
torsion  of  the  neck  and  an  extension  of  the  extremi- 
ties. They  occur  spontaneously,  but  are  more  marked 
when  the  animal  attempts  to  execute  any  voluntary 
movement.  The  forced  movements  are,  of  course, 
caused  by  muscular  action,  yet  there  is  neither  paraly- 
sis nor  spasticity  of  either  side  of  the  body.  It  fol- 
lows, then,  that  these  sj^mptoms  are  not  simple  motor 
phenomena  such  as  would  follow,  for  instance,  unilat- 
eral section  of  the  spinal  cord.  They  result  from  a 
peculiar  combination  of  muscular  activity  and  this 


PHYSIOLOGY  OF  CEREBELLUM      53 

combination  is,  in  all  probability,  the  province  of  the 
cerebellum. 

The  cerebellum  sends  out  a  continuous  stream  of 
impulses  which  result  in  a  condition  of  tonicity  of  the 
body  musculature.  Following  a  lesion  in  one  cere- 
bellar hemisphere  the  impulses  from  the  normal 
half  predominate,  and  thus  produce  the  forced  move- 
ments. 

As  the  period  of  forced  movements  comes  to  a  close 
and  the  animal  makes  efforts  to  stand  and  to  walk,  it 
becomes  apparent  that  there  is  marked  difficulty  in 
holding  the  body  erect  while  standing  and  in  main- 
taining equilibrium  during  progression.  This-  is  the 
period  of  incoordination.  The  cerebellum  is  there- 
fore an  important  organ  in  the  process  of  equilibra- 
tion and  its  destruction  experimentally  in  animals  or 
by  disease  in  man  entails  a  serious  disturbance  of  body 
balance. 

According  to  Lewandowsky  equilibration  results 
from  the  combined  activities  of  the  muscles  of  the 
trunk,  head,  eyes,  and  extremities.  It  consists  of 
maintenance  of  the  body  erect  in  space  against  the 
force  of  gravity  and  in  the  possibility  of  holding  a 
certain  direction  of  movement.  It  stands  in  close  rela- 
tionship to  the  ability  to  compensate  for  passive  rota- 
tion of  the  body  and  head  about  their  axis. 

If,  then,  we  consider  the  phenomena  following  le- 
sions of  the  cerebellum  as  disturbances  of  the  orienta- 


54  CEREBELLAR  ABSCESS 

tion  of  the  body,  we  have  confronting  us  the  ques- 
tions : 

1.  Through  which  peripheral  organs  and  b}-  what 
centripetal  pathways  are  the  factors  of  such  orienta- 
tion carried  to  the  cerebellum? 

2.  AVhat  processes  are  aroused  in  the  cerebellum? 

3.  Through  what  centrifugal  pathways  are  these 
impulses  carried  from  the  cerebellum,  and, 

4.  What  part  does  the  cerebrum  play  in  the  per- 
formance of  this  function  of  orientation  ? 

Equilibration  is  the  result  partly  of  conscious  im- 
pressions and  partly  of  reflex  activities.  The  reflex 
element  is  probably  the  more  important  of  the  two. 
The  conscious  elements  which  enter  into  the  main- 
tenance of  equilibrium  are  vision,  touch,  and  to  a 
lesser  extent  hearing  and  smell.  While  our  knowl- 
edge of  circumferential  space  is  gained,  to  a  certain 
extent,  from  these  sources,  it  is  locomotion  which 
really  enables  us  to  learn  the  details  of  space  and  it  is 
by  the  translation  of  our  bodies  and  limbs  that  we  ex- 
perience and  remember  the  depths  and  distances  that 
separate  us  from  any  definite  point  in  any  plane  of 
the  space  surroimding  us.  Our  knowledge  of  move- 
ments of  the  head  is  obtained  through  the  interme- 
diation of  a  special  organ  of  orientation,  viz.,  the 
static  labyrinth. 

As  the  result  of  the  information  received  from  these 
various  conscious  impressions  we  perform  voluntary 


PHYSIOLOGY  OF  CEREBELLUM      5ry 

movements  in  order  to  place  our  bodies  in  certain  posi- 
tions and  to  move  about  in  space.  These  voluntary 
movements  result  from  impulses  which  arise  from 
the  motor  area  of  the  cerebral  cortex  and  pass  through 
the  internal  capsule  and  pyramidal  tracts  to  the  an- 
terior horn  cells  of  the  cord.  From  here  they  pass 
through  the  anterior  nerve  roots  to  the  muscles  of 
the  head,  trunk  and  extremities. 

But  much  more  important  than  these  conscious 
impressions  and  voluntary  impulses  in  the  perform- 
ance of  orderly  movements  and  the  preservation  of 
body  balance  are  the  reflex  activities  of  the  cere- 
bellum. If  we  consider  the  important  peripheral 
sources  from  which  knowledge  of  our  spatial  rela- 
tions is  derived  we  find  that  they  consist  of  the  skin, 
muscles,  joints  and  the  static  labyrinth.  Without 
doubt,  the  recorded  memory  of  space,  so  far  as  knowl- 
edge is  attained  by  locomotion,  by  exploratory  move- 
ments of  our  limbs,  by  our  sense  of  touch  and  from 
the  static  labyrinth,  finds  its  physical  location  in  the 
kinesthetic  area  of  the  cerebral  cortex.  Across  the 
nerve  pathways,  in  a  sense,  which  transmit  impulses 
from  these  peripheral  sources  to  the  cerebral  cortex 
the  cerebellum  stands  as  the  center  of  a  reflex  arc. 
To  it  are  conveyed  impulses  from  the  skin,  muscles, 
joints  and  static  labyrinth,  and  from  it  emanate  im- 
pulses which  reflexly  establish  and  maintain  equi- 
librium. 


56  CEREBELLAR  ABSCESS 

From  the  muscles,  articular  surfaces,  ligaments  and 
tendons  impulses  are  constantly  being  transmitted  to 
the  cerebellar  cortex  through  the  posterior  nerve  roots 
and  Flechsig's  and  Gowers'  tracts.  These  impulses 
arise  even  when  the  body  is  at  rest.  From  the  skin 
impulses  are  sent  to  the  cierebellar  cortex  through  the 
posterior  nerve  roots  and  the  columns  of  Goll  and 
Burdach.  From  the  static  labyrinth  impulses  are  sent 
to  the  cerebellum  through  the  vestibular  nei^ves  and 
Deiters'  and  Bechterew's  nuclei.     (Fig.  12.) 

These  afferent  impulses  are  gathered  together  in 
the  cerebellar  cortex  and  are  projected  along  the 
axons  of  the  Purkinje  cells  to  the  central  nuclei.  In 
the  latter  secondary  impulses  arise  which  are  trans- 
mitted to  the  so-called  nucleus  motorius  tegmenti. 
This  is  composed  of  a  column  of  cells  in  the  tegmen- 
tum of  the  mid-brain,  pons  and  medulla,  of  which  the 
principal  enlargements  are  situated  at  the  red  nucleus 
in  the  mid-brain  and  Deiters'  nucleus  in  the  pons. 
From  the  cerebellar  nuclei  impulses  reach  the  oppo- 
site red  nucleus  via  the  brachium  conjunctivum.  They 
reach  the  opposite  nucleus  of  Deiters'  by  way  of  the 
tractus  uncinatus.  From  the  red  nucleus  the  im- 
pulses, crossing  again,  pass  through  the  rubrospinal 
or  Monakow's  tract  to  the  anterior  horn  cells.  From 
Deiters'  nucleus  they  pass  through  the  Deiterso-spinal 
tract  to  the  anterior  horn  cells.  Through  the  anterior 
nerve  roots  the  impulses  reach  the  muscles.    Thus  the 


PHYSIOLOGY  OF  CEREBELLUM     57 

reflex  arc  is  completed.  As  these  centrifugal  tracts 
cross  twice  between  the  cerebellar  hemisphere  and  the 
anterior  horn  cells  the  effect  is  homolateral. 

With  regard  to  the  question  as  to  what  processes 
are  aroused  in  the  cerebellum  as  the  result  of  the  affer- 


CER 


Fig.  12. — Cerebellar  Reflex  Arc. 

^I,  ^luscles.  CER,  Cerebellum. 

J,  Joints.  RN,  Red  nucleus. 

S,  Skin.  DN,  Deiters'  nucleus. 

C.  Semicircular  canals.  AHC,   Anterior    horn    cell. 


ent  impulses,  there  is  no  doubt  that  the  cerebellum 
originates  motor  impulses.  That  these  impulses  are 
independent  of  the  cerebrum  has  been  shown  often  in 
rabbits  in  which  the  cerebrum  was  removed  in  toto  and 
then  the  cerebellum  exposed  and  irritated  electrically. 
In  dogs  too,  after  removal  of  the  motor  centers  of  the 
extremities  in  the  cerebrum,  cerebellar  irritation  was 


58  CEREBELLAR  ABSCESS 

followed  by  motor  effects.  As  was  pointed  out  in 
discussing  forced  movements,  the  cerebellar  processes 
which  result  from  afferent  impulses  are  not  simple 
motor  phenomena. 

The  various  centripetal  impulses  from  muscles, 
joints,  skin  and  static  labyrinth  result  in  a  continuous 
stream  of  centrifugal  impulses  which  produce  a  cer- 
tain tonus  in  the  muscles  of  the  body.  The  purpose  of 
this  muscular  tonus  or  tension  is  to  preserve  the  body 
balance.  The  tension  in  the  muscles  of  one  side  of 
the  body  counterbalances  that  in  the  muscles  of  the 
opposite  side  and  thus  equilibrium  is  preserved.  As 
the  muscles  and  joints  are  moved  and  as  the  position 
of  the  head  is  changed,  the  various  centripetal  im- 
pulses change  and  result  in  corresponding  changes  in 
the  centrifugal  portion  of  the  reflex  arc.  In  this  way 
the  tension  in  the  muscles  of  different  parts  of  the 
body  is  altered  to  meet  the  new  conditions. 

When  there  is  a  lesion  in  one  half  of  the  cerebellum 
the  impulses  on  that  side  are  diminished  and  those 
from  the  opposite  side  overbalance.  The  result  is  a 
disturbance  of  equilibrium  and  the  production  of  the 
so-called  forced  movements.  When  these  disturbances 
occur  in  the  trunk  muscles  they  result  in  falling. 
A^Tien  they  occur  in  the  muscles  of  the  extremities 
they  result  in  deviations  of  the  extremities  or  the  so- 
called  "pointing  by."  These  disturbances  of  equilib- 
rium maj^  result  from  abnormalities  in  the  centripetal 


PHYSIOLOGY  OF  CEREBELLUM     59 

impulses  as  well  as  from  lesions  in  tlie  cerebellum 
itself,  as,  for  instance,  in  disease  of  the  static  laby- 
rinth or  Axstibular  nerve  or  from  lesions  of  the  pos- 
terior nerve  roots  of  the  spinal  cord.  They  may  also 
occur  from  abnormally  strong  centripetal  impulses 
such  as  are  aroused  by  the  rotation  or  caloric  tests. 

Horsley  and  Clark  have  shown,  by  their  experi- 
ments on  the  electrical  stimulation  of  the  cerebellum, 
that  the  closer  the  current  is  applied  to  the  central 
nuclei,  the  greater  is  the  reaction.  The  conclusions 
"which  they  draw  correspond  with  Edinger's  view,  viz. : 
That  the  cerebellar  cortex  is  purely  sensory.  Roth- 
mann  and  Shimazono,  on  the  contrary,  believe  that 
they  have  aroused  motor  phenomena  from  stimula- 
tion of  the  cerebellar  cortex  alone.  Probably  these 
views  differ  apparently  more  than  really.  Rothmann 
himself  in  discussing  the  division  of  the  brachium  and 
the  accessory  brachium  at  the  red  nucleus  states: 
"They  probabh^  convey  the  same  impulse.  The  for- 
mer through  the  rubrospinal  tract,  however,  results 
in  motion  earlier  than  the  latter  which  passes  to  the 
thalamus  and  so  to  the  cerebral  cortex."  There  is 
then,  in  all  probability,  no  great  essential  difference 
between  the  impulses  which  the  cerebellar  cortex  orig- 
inates and  those  which  emanate  from  its  central 
nuclei. 

E dinger  divides  the  cerebellum  on  physiological  as 
well  as  anatomical  grounds  into  a  paleo-  and  neo- 


60  CEREBELLAR  ABSCESS 

cerebellum.  To  the  paleo-cerebellum,  i.  e.,  the  vermis, 
he  ascribes  the  principal  part  in  the  development  of 
what  he  calls  the  statotonus,  i.  e.,  such  tonic  influences 
over  the  muscles  as  enable  them  to  maintain  the  body 
erect  while  standing  and  during  progression. 

To  the  experiments  of  Bing  w^e  owe  our  knowl- 
edge of  the  fact  that  the  afferent  impulses  from  the 
muscles,  joints  and  tendons  which  arouse  the  stato- 
tonus in  the  vermis  pass  to  the  latter  through  the  spino- 
cerebellar tracts.  These  tracts,  as  is  well  known,  end 
almost  exclusively  in  the  cortex  of  the  vermis.  Bing, 
pointing  out  the  danger  of  ambiguity  and  confusion 
in  the  interpretation  of  the  symptom-complex  follow- 
ing surgical  experiments  upon  the  cerebellum  itself, 
urged  the  reduction  of  the  problem  of  cerebellar  phj's- 
iology  to  it  utmost  simplicity.  Following  this  dictum 
he  destroyed  the  continuity  of  Flechsig's  and  Gowers' 
tracts  in  the  cord  and  observed,  as  a  sequence,  a 
marked  disturbance  in  the  statotonus. 

With  this  view  of  the  physiological  activity  of  the 
vermis  Barany  also  agrees,  and  he  ascribes  the  reac- 
tion movements  of  the  body  following  vestibular  im- 
pulses to  the  intermediation  of  the  cortex  of  the  ver- 
mis. Neither  pathological  nor  experimental  proof, 
however,  has  as  yet  fully  confirmed  this  theory. 

Rothmann,  in  discussing  Edinger's  theory,  holds 
that  the  statotonic  mechanism  is  solely  the  province 
of  the  paleo-cerebellum,  i.  e.,  the  vermis.    AYith  the 


PHYSIOLOGY  OF  CEREBELLUM      61 

development  of  the  neocerebellum,  i.  e.,  the  lateral 
hemispheres,  in  the  higher  mammals,  there  occurs  in 
the  cerebellum  a  mechanism  for  the  control  of  move- 
ments of  the  extremities  in  various  directions.  Clin- 
ically we  have  long  known  that  one  of  the  most  valu- 
able signs  of  cerebellar  disease  is  the  loss  of  power  to 
carry  the  hand  to  any  definite  point  in  a  coordinate 
manner.  In  the  study  of  this  phenomenon  and  the 
effect  of  vestibular  impulses  upon  movements  of  the 
limbs  Barany  has  evolved  a  theory  of  cerebellar  local- 
ization. 

He  believes  that  the  various  body  muscles  are  not 
represented  in  the  cerebellar  cortex  as  they  are  in  the 
cerebral  cortex,  but  that  in  the  former  the  muscles  are 
grouped  into  direction  centers.  Within  these  centers 
there  is  a  subdivision  according  to  joints  and  accord- 
ing to  the  position  of  joints.  In  each  half  of  the 
cerebellum  there  are  four  direction  centers;  one  for 
movement  upwards,  one  for  movement  downwards, 
one  for  movement  to  the  right  and  one  for  movement 
to  the  left.  In  the  center  for  movement  to  the  right 
there  are  centers  for  the  shoulder,  ^^^nst  and  hip 
joints,  etc.,  and  in  the  center  for  the  wrist  joint  there 
is  a  center  for  movement  with  the  hand  in  pronation 
and  one  for  movement  with  the  hand  in  supination. 

When  there  is  a  lesion,  for  example,  in  the  center 
for  movement  inward  at  the  shoulder  joint,  the  arm 
of  that  side  will  deviate  outward.    This  deviation  can 


62  CEREBELLAR  ABSCESS 

be  elicited  only  during  voluntary  motion,  as  when  the 
arm  is  held  extended,  or  when  an  attempt  is  made  to 
point  to  some  object.  The  deviation  is  most  marked 
when  the  eyes  are  closed,  for  if  the  patient  becomes 
aware  of  his  deviation  he  makes  a  voluntary  effort  to 
correct  it.  The  deviation  is  greatest  after  sudden  de- 
struction of  a  center.  After  a  certain  time  it  may  dis- 
appear as  the  result  of  compensation,  some  other  part 
of  the  cerebellum  or  some  other  part  of  the  central 
nervous  system  taking  up  the  function  of  the  destroj^ed 
area. 

Disturbance  of  the  centripetal  impulses  such  as 
occurs  with  stimulation  or  destruction  of  a  static 
labyrinth  will  give  rise  to  deviations  which  are  very 
similar  to  those  produced  by  destruction  of  the  cere- 
bellar centers. 

When,  as  a  result  of  stimulation  of  the  semicircular 
canals  in  an  individual  with  a  normal  cerebellum,  a 
labyrinthine  nystagmus  is  aroused,  there  will  occur  a 
deviation  of  all  four  extremities  in  the  plane  of  the 
nystagmus  and  in  the  direction  of  its  slow  compo- 
nent. This  is  called  the  pointing  reaction.  But  when 
there  is  a  cerebellar  lesion,  the  extremity"  effected  by 
the  lesion  will  point  correctly  in  the  presence  of  a 
vestibular  nystagmus.  In  other  words  there  is  a  loss 
of  the  pointing  reaction.  A  lesion  in  one  cerebellar 
hemisphere  causes  a  deviation  and  a  loss  of  the  point- 
ing reaction  only  in  the  extremities  of  the  same  side. 


PHYSIOLOGY  OF  CEREBELLUM      63 

For  example,  witli  a  lesion  in  the  right  cerebellar 
hemisphere  involving  the  center  for  movement  to  the 
left  of  the  shoulder  joint,  the  right  arm  extended  in 
front  of  the  body  would  deviate  to  the  right ;  the  left 
arm  would  point  correctly.  If,  now,  a  horizontal  nys- 
tagmus to  the  right  is  produced  either  by  cold  irriga- 
tion of  the  left  ear  or  by  rotation  to  the  left,  the  right 
arm  would  point  correctly  whereas  the  left  arm,  which 
received  the  stimuli  from  the  intact  cerebellar  hemi- 
sphere, would  deviate  to  the  left. 

When  the  lesion  of  the  cortex  is  a  large  one  many 
joints  will  be  involved  in  the  deviation;  when  the 
lesion  is  small  only  one  or  two  joints  will  be  involved. 

If  a  caloric  test  is  used  to  arouse  the  reaction  move- 
ments, the  head  should  be  tilted  backward  about  sixty 
degrees  in  order  to  elicit  a  horizontal  nystagmus.  In 
this  way  lateral  deviations  of  the  extremities  are  pro- 
duced. If  a  cold  caloric  is  done  in  the  left  ear  and 
the  head  held  upright,  a  mixed  rotatory  and  horizon- 
tal nystagmus  to  the  right  will  occur.  If  the  arms  are 
held  in  front  of  the  body,  they  will  deviate  to  the  left. 
If  the  right  arm  is  extended  laterally,  it  will  deviate 
upward.  If  the  left  arm  is  extended  laterally,  it  will 
deviate  downward.  If  the  head  be  now  rotated  to 
the  right  shoulder,  both  arms  held  in  front  of  the  body 
will  deviate  downward.  If  the  head  be  rotated  to  the 
left  shoulder,  both  arms  held  in  front  of  the  body  will 
deviate  upward.     It  is  clear,  from  these  facts,  that 


64  CEREBELLAR  ABSCESS 

the  deviations  are  dependent  upon  impulses  which 
arise  from  the  static  labyrinth  and  from  the  muscles 
and  joints  of  the  neck.  These  impulses  are  mixed,  as 
it  were,  in  the  cerebellar  cortex  and  there  arouse 
processes  which  influence  the  voluntary  impulses  from 
the  cerebrum.  In  this  way  the  reaction  movements  or 
deviations  occur.  The  deviation  is  always  in  the  plane 
of  the  nystagmus  and  in  the  direction  of  the  slow  com- 
ponent of  the  latter. 

When  there  is  spontaneous  deviation  but  no  loss 
of  reaction  movement  in  response  to  vestibular  stmi- 
ulation,  the  lesion  is  probably  remote  and  causes  im- 
pairment of  function  by  pressure  and  not  by  actual 
destruction  of  the  center. 

A  deviation  of  the  right  arm  to  the  right  may  be 
due  either  to  destruction  of  the  right  center  for  in- 
ward tonus  of  the  shoulder  joint,  or  to  hyperstimula- 
tion  of  the  right  center  for  outward  tonus  of  the  shoul- 
der joint.  In  order  to  determine  which  of  these  con- 
ditions is  present,  the  reaction  movements  of  the  right 
arm  should  be  compared  with  those  of  the  left  arm. 
If  the  reaction  movement  to  the  left  of  the  right  arm 
is  wanting,  there  is  destruction  of  the  right  center  for 
inward  tonus.  If  the  reaction  movement  to  the  right 
of  the  right  arm  is  greater  than  that  of  the  left  arm, 
tliere  is  hyperexcitability  of  the  right  center  for  out- 
ward tonus  of  the  shoulder. 

When  the  deviation  is  in  one  direction  only  and 


PHYSIOLOGY  OF  CEREBELLUM      65 

with  increase  in  intracranial  pressure  it  spreads  to  all 
joints  without  taking  a  new  direction  there  is,  in  all 
probability,  a  cortical  cerebellar  lesion.  This  is  anal- 
ogous to  monoplegia  resulting  from  a  lesion  in  the 
cerebral  cortex.  When  the  deviation  and  the  loss  of 
reaction  movements  is  in  more  than  one  direction 
there  is  probably  a  lesion  in  the  central  portion  of  the 
cerebellum  involving  the  fiber-tracts. 

Lesions  of  the  cerebellar  hemispheres  cause  devia- 
tions of  the  extremities.  Lesions  of  the  central  lobe 
or  vermis  cause  disturbances  of  the  trunk  muscles  with 
loss  of  equilibrium.  If  an  artificial  rotatory  nj^s- 
tagmus  is  aroused  bj^  means  of  cold  or  hot  water  in 
the  ear,  the  patient  falls  in  the  direction  of  the  slow 
component  of  the  nystagmus  when  the  vermis  is 
intact.  For  example,  if  a  cold  caloric  is  done  in  the 
right  ear  the  patient  falls  to  the  right.  If  the  head 
be  turned  to  the  left  shoulder  he  falls  forward.  If 
the  head  be  turned  to  the  right  shoulder  he  falls  back- 
ward. As  the  reaction  movements  of  the  extremities, 
so  the  reaction  movements  of  the  trunk  are  dependent 
upon  impulses  from  the  static  labyrinth  and  from  the 
muscles  and  joints  of  the  neck.  They  are  always  in 
the  plane  of  the  nystagmus  and  in  the  direction  of 
the  slow  component  of  the  latter. 

If  there  is  a  lesion  of  the  vermis,  there  is  spon- 
taneous falling,  usually  toward  the  side  of  the  lesion. 
The  direction  of  this  spontaneous  falling  will  not  be 


66 


CEREBELLAR  ABSCESS 


changed  by  the  production  of  a  caloric  vestibular  reac- 
tion. In  other  words,  the  "falling  reaction"  is  want- 
ing.    The  loss  of  the  falling  reaction  may  be  in  one 


Fig.    13. — Cerebellum,  Lateral   View. 
IW,  Center  for  inward  tonus  of  wrist. 
IS,  Center  for  inward  tonus  of  shoulder. 
IH,  Center  for  inward  tonus  of  hip. 
OS,  Center  for  outward  tonus  of  shoulder. 
PS,  Postero-superior  lobe. 
PI,   Postero-inferior  lobe. 
GHS,  Great  horizontal  fissure. 
BV,  Biventral  lobe. 


or  several  directions.  In  tlie  latter  case  the  lesion 
would  be  larger  or  more  centrally  located  than  in  the 
former  case. 


PHYSIOLOGY  OF  CEREBELLU:M      67 

Whether  we  agree  with  Barany's  conclusions  or 
not,  w^e  cannot  deny  the  results  of  his  experiments  of 
freezing  parts  of  the  cerebellar  cortex,  for  they,  too, 
reduce  the  problem  of  cerebellar  physiology  to  its 
elements. 

By  means  of  freezing  portions  of  the  cerebellar 
cortex  as  well  as  through  operative  and  pathological 
lesions  of  the  cerebellum,  Barany  was  able  to  map  out 
definite  tonus  centers.  He  found  that  there  is  a 
region  in  the  cortex  of  the  biventral  lobe,  just  behind 
that  portion  of  the  cerebellum  which  lies  against  the 
internal  auditory  meatus,  which  controls  inward  move- 
ment of  the  wrist  joint.  (Fig.  13.)  The  center  for 
position  w^ith  the  palm  downward  is  located  in  the 
medial  portion  of  this  area  and  that  for  position  with 
the  palm  upward  in  the  lateral  portion.  A  little 
behind  and  above  this  area  is  the  center  which  con- 
trols inward  movement  of  the  shoulder  joint,  and  just 
behind  this,  the  center  which  controls  inw^ard  move- 
ment of  the  hip  joint. 

By  freezing  the  shoulder  area  he  has  repeatedly 
shown  that  there  follows  a  spontaneous  deviation  of 
the  arm  of  the  affected  side  outward  and  a  loss  of 
the  pointing  reaction  of  that  arm  inward.  In  twenty 
cases  of  pathological  and  operative  lesions  of  this  area 
the  same  phenomena  were  observed.  Near  the  pos- 
terior pole  of  the  cerebellar  hemis])here,  viz.,  at  the 
medial    end    of    the    postero-superior    and    postero- 


68 


CEREBELLAR  ABSCESS 


inferior  lobes,  is  the  center  for  downward  movement 
of  the  shoulder  joint,  and  three  to  four  centimeters 
outward  from  this  point,  at  the  edge  of  the  hemi- 
sphere, viz.,  at  the  middle  of  the  postero-superior  and 
postero-inferior  lobes,  is  the  center  for  outward  move- 
ment of  the  shoulder  joint.      (Eig.  14.) 


QriF 


Fig.  14. — Cerebellum,  Posterior  View, 
DS,  Center  for  inward  tonus  of  shoulder. 
OS,  Center  for  outward  tonus  of  shoulder. 
PS,  Postero-superior  lobe. 
GHF,  Great  liorizontal  fissure. 
PI,  Postero-inferior  lobe. 


We  come  now  to  the  fourth  question  which  we  have 
propounded  for  ourselves,  viz.,  what  part  does  the 
cerebrum  play  in  this  function  of  static  orientation? 
There  is  no  question  that  conscious  impulses  enter  into 
the  maintenance  of  body  balance,  for  during  uncon- 
sciousness equilibrium  is  abolished.  Yet  the  processes 
which  serve  this  purpose  are  carried  on  in  the  subcon- 


PHYSIOLOGY  OF  CEREBELLUM      69 

scious  plane.  The  voluntary  impulses  which  are  used 
for  maintaining  equilibrium  and  for  controlling  the 
movements  of  the  extremities  pass  into  the  cerebellum 
via  the  middle  cerebellar  peduncles.  In  the  cerebel- 
lum they  meet  the  centripetal  impulses  from  the  mus- 
cles, joints,  skin  and  static  labyrinth.  These  centrip- 
etal impulses  modify  the  motor  cerebral  impulses  in 
such  a  wajT-  as  to  make  them  efficacious  in  preserving 
body  balance.  The  cerebrimi  originates  the  move- 
ments and  the  cerebellum  carries  them  out. 

The  cerebellum  exercises  an  inhibitory  control  over 
the  vestibular  centers  and  also  over  the  motor  areas 
in  the  cerebral  cortex.  That  it  exercises  an  inhibitory 
control  over  the  vestibular  centers  is  shown  by  the 
following  fact.  If  with  a  normal  cerebellum  a  cold 
caloric  is  done  and  the  flow  stopped  as  soon  as  nys- 
tagmus sets  in,  the  nystagmus  will  continue  for  one 
or  two  minutes.  In  cerebellar  disease,  the  caloric 
nystagmus  which  is  directed  toward  the  affected  hemi- 
sphere will  continue  for  five  or  ten  minutes  or  even 
longer  and  is  much  more  intense  than  usual.  This  has 
been  called,  by  Xeumann,  "enduring  nystagmus." 
That  the  cerebellum  exercises  an  inhibitory  control 
over  the  motor  area  in  the  cerebral  cortex  was  shown 
by  I.  L.  Meyers  in  the  following  ingenious  way:  Ex- 
cited tissue  is  electricalh^  negative  in  relation  to  quies- 
cent tissue.  The  galvanic  current  travels  from  the 
quiescent  to  the  active  part,  i.  e.,  from  the  positive  to 


70  CEREBELLAR  ABSCESS 

the  negative  pole  in  the  external  circuit.  In  the  tis- 
sue portion  of  the  circuit  it  travels  from  the  active 
to  the  quiescent  part.  When  half  of  the  cerebellum 
was  removed,  in  a  cat,  and  both  sciatic  nerves  exposed 
and  joined  together  by  means  of  a  wire,  in  the  course 
of  which  a  galvanometer  was  interposed,  the  deflec- 
tion of  the  galvanometer  needle  showed  that  the  nerve 
on  the  side  of  the  cerebellar  lesion  was  negative,  and 
the  one  on  the  sound  side  positive.  In  other  words, 
the  nerve  on  the  side  of  the  lesion  was  in  a  state  of 
hyperexcitabilitj^  When  the  contralateral  motor 
area  in  the  cerebrum  was  removed  the  galvanometer 
deflection  ceased.  This  proves  that  the  cerebellar 
hemisphere  exercises  an  inhibitory  control  over  the 
opposite  motor  area  in  the  cerebrum.  But  that  the 
cerebellum  has  motor  functions  independent  of  the 
cerebrum  was  shown  by  Rothmann,  who  removed  the 
cerebrum  in  rabbits  and  was  still  able  to  produce  mus- 
cular contraction  by  electrical  stimulation  of  the 
cerebellum. 

That  the  cerebellum  has  a  tonic  influence  on  the 
musculature  of  the  body  is  shown  by  the  hypotony 
lUid  atony  that  ensue  from  cerebellar  disease  and  from 
experimental  lesions  of  the  cerebellum  in  animals. 

The  various  disturbances  which  occur  as  a  result 
of  lesions  of  the  cerebellum  are  most  marked  immedi- 
ately after  the  lesion  has  occurred.  They  gradually 
diminish  in  intensity  and  in  some  cases  entirely  dis- 


PHYSIOLOGY  OF  CEREBELLUM      71 

appear  in  time.  This  is  due  to  the  fact  that  the  func- 
tion of  the  injured  portion  of  the  cerebellum  is  taken 
up  either  by  some  other  part  of  the  cerebellum  or  by 
some  other  part  of  the  central  nervous  system.  When 
the  lesion  in  the  cerebellum  is  produced  very  slowly 
there  may  be  no  symptoms  whatever,  compensation 
keeping  pace  with  the  destruction.  In  the  cases  of 
animals  with  cerebellar  lesions  who  have  regained  their 
equilibrium,  destruction  of  the  motor  cerebral  cortex 
causes  a  recurrence  of  the  loss  of  equilibrium.  That 
other  portions  of  the  cerebellum  compensate  for  the 
destroyed  portions  is  proven  by  the  following  fact: 
If  one  inferior  peduncle  is  destroyed  in  a  dog,  there 
occur  rolling  movements  around  the  antero-posterior 
axis  of  the  body  toward  the  operated  side.  If  the 
other  inferior  peduncle  is  then  divided,  the  rolling 
movements  cease  and  symptoms  of  static  incoordina- 
tion appear.  If,  however,  after  section  of  the  first 
side,  sufficient  time  is  allowed  to  elapse  for  compen- 
sation to  take  place,  and  then  the  second  side  is 
divided,  there  occur  rolling  movements  toward  the 
newly  operated  side. 


CHAPTER  III 

ETIOLOGY  AND   PATHOLOGY   OF   CEREBELLAR  ABSCESS 


CHAPTER  III 

ETIOLOGY    AND    PATHOLOGY    OF    CEREBELI-AR   ABSCESS 

CEREBELLAR  abscess  is,  in  the  vast  ma- 
jority of  instances,  otitic  in  origin.  Of 
eiglity-six  cases  of  cerebellar  abscess  col- 
lected from  the  literature  since  1907,  eighty-five 
were  due  to  suppuration  within  the  temporal  bone. 
The  remaining  case  was  traumatic  in  origin.  Among 
other  causes  may  be  mentioned  abscess  or  gangrene 
of  the  lung,  purulent  bronchitis,  empyema,  purulent 
pericarditis,  compound  fractures,  pyemia  and  tuber- 
culosis. 

Cerebellar  abscess  ma}^  complicate  either  an  acute 
or  a  chronic  suppuration  of  the  middle  ear  and  mas- 
toid. It  is,  however,  far  more  frequently  associated 
with  the  chronic  otitides.  In  the  eighty-six  cases  col- 
lected, fourteen  (16.2  per  cent)  complicated  the  acute 
otitides,  while  seventy-two  (83.8  per  cent)  followed 
the  chronic  suppurations.  Okada  found  acute  mid- 
dle-ear suppuration  as  the  causative  factor  in  twenty- 
eight  cases  (19  per  cent)  of  cerebellar  abscess,  and 
chronic  middle-ear  suppuration  in  one  hundred  and 
twenty  cases  (81  per  cent) . 

Heimann  found  20  per  cent  following  acute  mid- 
75 


76  CEREBELLAR  ABSCESS 

die-ear  suppuration  and  80  per  cent  following  chronic 
suppuration.  Neumann  found  12  per  cent  following 
acute  suppuration  and  88  per  cent  following  chronic 
suppuration. 

Grunert  found  9  per  cent  following  acute  suppu- 
ration and  91  per  cent  following  chronic  suppura- 
tion. 

Hammerschlag  found  25  per  cent  following  acute 
suppuration  and  75  per  cent  following  chronic  suppu- 
ration. 

The  reason  for  this  undoubtedly  lies  in  the  fact  that 
in  the  chronic  cases,  there  is  gi-eater  destruction  of 
bone,  prolonged  interference  with  drainage  and  the 
presence  of  cholesteatoma.  Thus  in  the  vast  majority 
of  instances  we  find  either  polypi,  cholesteatoma  or 
small  tympanic  perforations  chiefly  in  Shi-apnell's 
membrane.  Furthermore,  in  chronic  suppurative 
cases,  there  usually  occurs  a  sclerosis  of  the  cortex 
which  favors  necrosis  of  the  deeper  lying  bony  struc- 
tures. It  is  particularly  in  those  instances  in  which 
cholesteatoma  has  eroded  the  bone  and  lies  in  direct 
contact  with  the  dura  that  intracranial  complications 
occur.  The  cholesteatoma  not  only  seriously  inter- 
feres with  drainage,  but  also  acts  as  an  excellent  me- 
dium for  the  groAvth  of  the  invading  microorganisms. 
In  acute  middle-ear  suppuration  the  mucous  mem- 
brane and  the  bony  walls  are  intact,  and  intracranial 
extension  occurs  onlv  when  the  infection  is  so  viru- 


ETIOLOGY  AND  PATHOLOGY        77 

lent  that  thrombi  are  formed  in  the  vessels  which  pass 
between  the  middle  ear  and  cranial  cavity.  Occasion- 
ally, in  acute  middle-ear  suppuration,  the  infection 
travels  through  the  labyrinthine  windows  to  the  in- 
ternal ear  and  then  through  the  internal  auditory 
canal  into  the  cranial  cavity.  In  such  cases,  however, 
meningitis  is  more  apt  to  result  than  cerebellar  ab- 
scess. 

According  to  most  authors  cerebellar  abscess  is  not 
as  common  as  abscess  in  the  temporo-sphenoidal  lobe. 
Koerner  found  69  cases  of  temporo-sphenoidal  lobe 
abscess  to  30  of  cerebellar  abscess.  Growers  found  186 
temporo-sphenoidal  lobe  abscesses  to  41  cerebellar. 
Le  Fort  and  Lehmann  found  327  temporo-sphenoidal 
lobe  abscesses  to  113  cerebellar.  JNIichaelsen  found 
cerebellar  abscess  to  be  as  frequent  as  temporo-sphe- 
noidal lobe  abscess.  Eight  of  his  cases  were  in  the 
cerebellum  and  eight  in  the  cerebrimi. 

INIales  are  attacked  much  more  frequently  than  fe- 
males, the  proportion,  in  our  series,  being  3:1. 

0-10       11-20        21-30        Over 
Avthor.  yrs.         yrs. 

Koch 11  33 

Okada 17  56 

Koerner 4  14 

Heimann  ....  16  57 

Neumann  ....  12  51 


yrs. 

30  yrs. 

3.5 

19 

45 

28 

12 

10 

38 

26 

41 

30 

78  CEREBELLAR  ABSCESS 

jSTeumanii  gives  the  above  statistics  on  the  rela- 
tive frequency  of  occurrence  of  cerebellar  abscess 
at  different  periods  of  life. 

In  the  series  we  have  collected,  it  occurs  with  great- 
est frequency  in  the  second  decennium,  and  with  least 
frequency  in  the  first  and  sixth  decennia,  while  in  the 
third,  it  occurs  about  as  frequently  as  it  does  in  the 
fourth  and  fifth  combined.  Thiis  in  the  86  cases,  6 
were  under  10,  29  were  between  10  and  20,  22  were 
between  20  and  30,  12  were  between  30  and  40,  10 
were  between  40  and  ,50,  and  5  between  50  and  60. 
In  2  the  age  w^as  not  stated.  It  occurred  45  times  on 
the  right  side  and  37  times  on  the  left.  In  4  the  side 
was  not  stated. 

With  regard  to  the  etiology  of  cerebellar  abscess, 
Neumann  differentiates  between  those  which  compli- 
cate the  acute  middle  ear  infections  and  those  occur- 
ring with  the  chronic  otitides.  Of  19  cases  of  cere- 
bellar abscess  following  acute  middle-ear  suppuration, 
the  description  was  so  imperfect  in  4  that  the  pathway 
of  infection  could  not  be  determined.  Of  the  remain- 
ing 15  cases,  8  were  due  to  sinus  thrombosis,  and  6  fol- 
lowed epidural  abscess  in  the  posterior  fossa.  In  one 
there  was  a  labyrinthitis,  but  it  could  not  be  positively 
determined  that  this  was  the  cause  of  the  abscess. 
Our  statistics  confirm  this  viewpoint.  In  the  14  cases 
of  cerebellar  abscess  complicating  acute  otitis  media 
and  mastoiditis,  sinus  thrombosis  occurs  in  6.    In  only 


ETIOLOGY  AND  PATHOLOGY        79 

one,  however,  is  there  a  direct  connection  evident,  mac- 
roscopically,  between  the  infected  sinus  and  the  cere- 
bellar abscess.  This  proportion  is  probably  too  low 
and,  in  other  statistics,  such  evidence  is  more  fre- 
quently met  with.  Although  in  the  majority  of  in- 
stances the  cerebellar  infection  is  secondary  to  the 
sinus  thrombosis,  this  does  not  seem  to  be  invariably 
so. 

Death  from  the  rupture  of  a  cerebellar  abscess  into 
the  lateral  sinus  has  been  reported,  and  the  fact  that 
symptoms  of  sinus  thrombosis  occur  late  in  some  of 
the  cases,  notablj"  those  of  Barr,  Beck  and  others, 
brings  to  mind  the  possibility  of  the  sinus  infection 
being  secondary  to  the  brain  abscess.  Histological 
proof  of  this  etiological  relationship  is  not  at  hand.  In 
four  of  the  acute  cases  an  epidural  abscess  in  the  pos- 
terior fossa  is  probably  the  pathway  of  the  endo- 
cranial  complication.  So  that  in  our  series,  too,  the 
route,  which  the  cerebellar  infection  follows,  in  the 
majority  of  cases  complicating  acute  otitis,  is  either 
from  a  thrombosed  sinus  or  an  epidural  abscess.  In  but 
one  of  the  acute  cases  (L^ffenorde)  was  the  labyrinth 
the  pathway  of  the  intracranial  infection.  This  was 
an  acute  middle-ear  infection  complicating  scarlet, 
and  the  cerebellar  abscess  resulted  from  an  extension 
of  a  saccus  empyema.  Here,  despite  the  virulence 
of  the  infection  and  the  lack  of  resistance  on  the  part 
of  the  individual  attacked,  the  intracranial  extension 


80  CEREBELLAR  ABSCESS 

from  the  suppurative  labyrinthitis  was  a  circum- 
scribed collection  of  pus,  i.  e.,  a  brain  abscess  and  not  a 
diffuse  purulent  meningitis. 

The  cerebellar  abscesses  which  complicate  the 
chronic  middle-ear  suppurations  differ  very  decidedly 
in  their  etiology  from  those  which  occur  with  the  acute 
otitides.  In  Neumann's  series,  there  are  132  cases  of 
cerebellar  abscess  complicating  chronic  suppurative 
otitis  media.  Twenty  are  so  incompletely  described 
that  they  are  worthless.  Of  the  remaining  112,  49, 
that  is  43.75  per  cent,  showed  labyrinthine  suppura- 
tion. Thirty-eight  were  due  to  sinus  thrombosis  and 
16  to  -extradural  abscess  of  the  posterior  fossa.  In  3 
cases  there  were  extradural  abscess  and  sinus  throm- 
bosis and  in  6  cases  there  were  labyrinthitis  and  sinus 
thrombosis.  In  the  series  collected  by  us,  31  of  the  72 
cases  with  chronic  purulent  otitis  showed  labyrin- 
thine suppuration.  These  figures,  startling  as  they 
are,  are  probably  an  underestimate  rather. than  an 
overestimate.  We  base  this  judgment  upon  the  fol- 
lowing facts.  If  we  examine  individual  reports  in- 
cluded in  our  series,  we  find  first  8  cases  reported  by 
Michaelsen.  Of  these,  6  are  cerebellar  abscesses  com- 
plicating chronic  suppurative  otitis  media.  In  these  6 
cases  "dead  labyrinth"  was  found  5  times.  Again 
Ruttin  reports  7  cases,  all  of  them  complicating 
chronic  suppurative  otitis.  In  six  of  the  seven,  laby- 
rinthine suppuration  occurred.     Neumann  reports  5 


ETIOLOGY  AND  PATHOLOGY        81 

cases,  all  of  them  complicating  chronic  purulent  oti- 
tis media.  In  these,  labyrinthine  suppuration  oc- 
curred three  times.  These  figures,  we  believe,  are  the 
result  of  careful  clinical  examination  and  are  not  ac- 
cidental. In  many  of  the  cases  the  labyrinthine  sup- 
puration was  proven  histologically. 

Undoubtedly,  there  is  a  small  proportion  of  cases 
of  cerebellar  abscess  in  which,  although  the  laby- 
rinth is  the  seat  of  a  suppurative  process,  it  is  not  the 
pathway  of  the  infection  from  the  middle  ear  to  the 
endocranial  structures.  In  a  case  which  we  recently 
had  an  opportunity  to  examine  post  mortem  and  in 
which  the  temporal  bone  was  examined  histologically, 
the  following  facts  presented.  Not  a  vestige  of  laby- 
rinthine endorgans,  auditory  or  static,  remained. 
There  was  a  fistula  in  the  external  semi-circular  canal 
filled  with  granulations  and  new-formed  connective 
tissue.  From  this  focus  the  labyrinth  probably  be- 
came infected.  The  crura  of  the  stapes  were  de- 
stroyed, but  the  foot-plate,  although  much  eroded, 
was  still  present  in  the  oval  window.  With  the  ex- 
ception of  this  fistula  in  the  external  semi-circular 
canal,  the  bony  canals  were  everj^where  intact.  There 
was,  furthermore,  no  erosion  of  the  inner  labyrin- 
thine wall.  The  internal  auditory  canal  contained  no 
pus.  The  pathway  of  the  intracranial  infection  could 
be  traced  through  the  inner  (posterior)  antral  wall. 
In  this  situation  there  was  an  epidural  abscess  and  a 


82  CEREBELLAR  ABSCESS 

perforation  led  through  the  bony  wall  and  through 
the  dura  to  the  cerebellar  abscess. 

In  our  series,  suppurative  labyrinthitis  and  epi- 
dural abscess  occurred  scA^en  times.  Thus  suppura- 
tive labyrinthitis,  epidural  abscess  and  cerebellar  ab- 
scess form  a  fairly  common  triad.  The  etiological  re- 
lationship between  these  three  factors  is  not  a  con- 
stant one.  While  it  is  natural  to  suppose  that  the 
epidural  abscess  is  secondary  to  the  suppurative  laby- 
rinthitis, this  is  not  invariably  so.  In  his  considera- 
tion of  the  relationship  between  deep  epidural  ab- 
scess in  the  posterior  fossa  and  suppurative  labyrinth- 
itis, Griinberg  reports  a  most  carefully  studied  case. 
The  labyrinth  was  the  seat  of  a  diffuse  suppurative 
process.  The  windows,  both  the  oval  and  the  round, 
were  intact.  The  labyrinthine  capsule  was  everywhere 
intact  with  the  exception  of  the  common  limb,  i.e.,  the 
junction  of  the  superior  with  the  posterior  semi-cir- 
cular canal.  At  this  point  there  was  an  erosion  from 
without  inward,  unquestionably  caused  by  the  epi- 
dural abscess  in  this  location. 

Ruttin  has  shown  that  in  mastoiditis,  particularly^ 
in  those  latent  varieties  due  to  infection  by  the  strepto- 
coccus mucosus,  there  is  a  tendency  to  necrosis  in  the 
deep  seated  petrosal  cells  surrounding  the  labyrin- 
thine capsule.  Drainage  from  this  region  is  particu- 
larly difficult  and  an  epidural  abscess  may  result.  It 
can  readily  be  understood,  then,  how  an  epidural  ab- 


ETIOLOGY  AND  PATHOLOGY        83 

scess  in  this  location  may  give  rise  to  cerebellar  ab- 
scess on  the  one  hand,  and  to  a  diffuse  labyrinthine 
suppuration  on  the  other., 

Formerl}^  in  many  of  these  cases  of  suppurative 
labyrinthitis,  epidural  abscess  and  cerebellar  abscess, 
a  saccus  empyema  was  adjudged,  upon  macro- 
scopical  findings,  the  pathway  of  the  cerebellar  infec- 
tion. INIacroscopical  findings,  however,  are  inade- 
quate to  establish  such  a  judgment.  The  microscope 
alone  is  the  final  arbiter.  In  order  to  diagnose  sac- 
cus empyema  it  is  necessary  to  demonstrate  an  epi- 
thelial lining  in  the  abscess  cavity.  In  those  cases  in 
which  the  cerebellar  abscess  is  secondary  to  a  saccus 
empyema,  there  is  a  likelihood  that  a  sinus  thrombosis 
is  also  present.  The  pus  in  the  saccus  gradually  ex- 
tends backward  between  the  two  layers  of  the  dura, 
this  being  the  direction  in  which  the  fibrous  tissue  con- 
necting the  layers  of  the  dura  is  least  dense. 
The  pus  eventually  comes  to  lie  in  the  inner  wall  of 
the  lateral  sinus.  In  this  situation  it  is  located  be- 
tween the  sinus  and  the  cerebellum.  The  infection 
may  extend  in  both  directions  causing  a  sinus  throm- 
bosis and  a  cerebellar  abscess.  When  the  clinical  ex- 
amination shows  symptoms  of  suppurative  labyrin- 
thitis, sinus  thrombosis  and  cerebellar  abscess,  the 
pathway  of  infection  is  usually  through  the  saccus. 
Kramm  and  Hegener  have  reported  such  cases  with 
histological  examination. 


84  CEREBELLAR  ABSCESS 

In  eight  cases,  suppurative  labyrinthitis  occurred 
■with  sinus  thrombosis.  In  only  one  of  these,  however, 
is  the  labyrinth  clearly  indicated  as  the  direct  path- 
way of  the  sinus  infection.  In  this  instance,  in  addi- 
tion to  the  sigmoid  sinus,  the  bulb,  inferior  petrosal 
and  cavernous  sinuses  were  also  thrombosed.  Here 
the  infection,  in  all  probability,  started  in  the  labyrin- 
thine veins,  extended  to  the  inferior  petrosal  sinus  and 
thence  forward  to  the  cavernous  and  backward  to  the 
bulb  and  sigmoid.  The  pathways  of  infection  from 
the  middle  ear  to  the  cerebellum  are  as  follows : 

1.  From  the  middle  ear  through  the  round  or  oval 
window  or  through  a  fistula  in  the  horizontal  semi- 
circular canal  or  promontory  to  the  internal  ear.  From 
here  through  a  fistula  in  the  posterior  petrosal  surface 
to  the  cerebellum. 

2.  From  the  middle  ear  to  the  labyrinth;  through 
the  internal  auditory  canal  to  the  cerebellum. 

3.  From  the  middle  ear  to  the  lab^^rinth;  through 
the  ductus  endolymphaticus  to  the  saccus.  From  here 
to  the  cerebellum. 

4.  From  the  middle  ear  to  the  labyrinth;  through 
the  aqueductus  cochleae  to  the  cerebellum. 

5.  From  the  middle  ear  to  the  antrum  and  mastoid 
cells;  through  the  inner  (posterior)  antral  wall  to 
the  lateral  sinus.    From  the  sinus  to  the  cerebellum. 

6.  From  the  middle  ear  to  the  antrum  and  mas- 
toid cells ;  through  the  inner  table  to  the  epidiu'al  space 


ETIOLOGY  AND  PATHOLOGY        85 

either  in  front  of  or  behind  the  sinus.  From  here  to 
the  cerebelhim. 

7.  From  the  middle-ear  to  the  facial  canal.  From 
here  to  the  cerebelhim. 

From  an  etiological  point  of  view  as  well  as  from  a 
pathological  and  clinical  point  cerebellar  abscess  may 
be  divided  into 

a.  Labyrinthogenic. 

b.  Non-labyrinthogenic. 

In  all  probability  at  least  50  per  cent  of  cerebellar 
abscesses  complicating  chronic  supprative  otitis  media 
are  labyrinthogenic.  In  a  small  proportion  of  cases, 
the  labyrinth  is  the  seat  of  diffuse  suppuration  and  is 
destroyed,  but  is  not  the  pathway  of  infection  to  the 
brain. 

On  the  other  hand,  of  those  cases  of  cerebellar  ab- 
scess which  complicate  the  acute  otitides,  from  90  to 
95  per  cent  are  non-labyrinthogenic,  i.  e.,  they  take 
origin  either  in  a  sinus  thrombosis  or  an  epidural  ab- 
scess of  the  posterior  fossa.  In  a  general  way,  middle- 
ear  infections  which  progress  to  the  intracranial  struc- 
tures through  natural  openings,  lead  to  a  diffuse  sup- 
purative process,  i.  e.,  meningitis,  whereas  those  that 
do  not  follow  preformed  paths  cause  circumscribed 
collections  of  pus,  i.  e.,  either  brain  or  subdural  ab- 
scesses. The  aqueductus  vestibuli  offers  a  notable 
exception  to  this  rule.  An  infection  traveling  along 
this  route  is  retarded,  probably  because  of  the  narrow 


86  CEREBELLAR  ABSCESS 

lumen  of  the  aqueduct,  the  facility  with  which  protec- 
tive adhesions  are  formed  and  the  fact  that  the  aque- 
duct ends  in  a  closed  sac  between  the  layers  of  a  very 
resistent  membrane,  viz.,  the  dura.  Such  infections, 
then,  frequently  lead  to  cerebellar  abscesses,  rarely 
through  a  saccus  empyema,  more  often  through  an 
erosion  of  the  bony  wall  of  the  aqueduct  and  the  for- 
mation of  an  epidural  abscess. 

Whether  the  labyrinth  infection  leads  to  a  diffuse 
meningitis  or  to  a  cerebellar  abscess  depends  upon  the 
virulence  of  the  infection.  In  this  regard  the  progress 
of  the  middle-ear  infection  into  the  labyrinth  is  of 
considerable  importance.  Slow,  erosive  processes,  de- 
stroying the  labyrinthine  capsule,  are  much  more  apt 
to  arouse  circumscribed  intracranial  complications 
than  are  labyrinthitides  in  which  infection  takes  place 
suddenly  through  the  windows. 

A  notable  example  is  the  case  reported  by  Thomp- 
son. In  this  instance,  cholesteatoma  had  eroded  both 
labyrinths,  and  the  latter  were  the  seat  of  diffuse  sup- 
puration. Each  lateral  cerebellar  lobe  contained  an 
abscess.  The  pathway  of  the  intracranial  infection 
was  along  the  nerves  in  the  internal  auditory  canal. 
That  the  pathway  of  the  infection  into  the  labyrinth 
may  be  of  importance  in  determining  the  character 
of  the  intracranial  complication  even  where  the  lat- 
ter occurs  wath  the  acute  otitides,  the  case  reported 
by  UfFenorde  illustrates.    Here  the  labyrinth  became 


ETIOLOGY  AND  PATHOLOGY        87 

infected  by  an  erosion  through  the  promontory  and 
not  by  the  windows. 

Of  the  hibyrinthogenic  cases  of  cerebellar  abscess, 
those  with  a  fistula  in  the  posterior  petrosal  wall  are 
by  far  the  most  common.  The  suppurative  process 
does  not  extend,  in  these  cases,  from  within  one  of 
the  semi-circular  canals  or  the  vestibule,  through  the 
posterior  petrosal  wall  by  a  process  of  erosion;  but 
the  sequence,  according  to  a  number  of  cases  examined 
histologically  by  Hegener,  is  as  follows :  As  a  result 
of  the  chronic  inflammatory  process  in  the  middle-ear 
(usually  with  cholesteatoma),  there  is  an  erosion  of 
the  labyrinthine  capsule  with  the  formation  of  a  fis- 
tula, most  commonh^  in  the  horizontal  semi-circular 
canal.  The  intralabyrinthine  space  becomes  filled 
with  pus  and  granulations,  the  membranous  labyrinth 
being  destroyed.  Following  extension  of  the  granu- 
lation tissue  into  the  fundus  of  the  internal  auditory 
canal,  the  internal  auditory  artery  becomes  occluded. 
As  this  artery  constitutes  the  entire  blood  supply  of 
the  internal  ear,  there  results  a  necrosis  of  the  bony 
labyrinthine  capsule.  This  dead  bone  sets  up  a  reac- 
tive inflammation  in  the  surrounding  spongy  bone  and 
very  soon  the  necrotic  labyrinthine  capsule  becomes 
enveloped  in  a  zone  of  granulation  tissue.  This  re- 
active inflammation  in  the  spongj'^  bone  surround- 
ing the  labyrinthine  capsule  gradually  extends  to  the 
posterior  petrosal  surface  and  finally  reaches  the  dura. 


88  CEREBELLAR  ABSCESS 

Cerebellar  abscess  is  usually  situated  near  the  ear 
which  is  the  origin  of  the  infection.  The  only  excep- 
tions to  this  rule  are  those  cases  in  which  the  ab- 
scesses are  pyemic  in  origin.  According  to  Koerner's 
statistics,  in  42  per  cent  of  the  cases  of  brain  abscess 
observed  by  him,  there  was  a  fistula  between  the  brain 
abscess  and  the  suppurating  focus  in  the  temporal 
bone.  In  1.5  per  cent  of  the  cases  the  brain  substance 
between  the  abscess  and  the  dura  was  broken  down  so 
that  only  the  dura  remained  between  the  abscess  and 
the  diseased  bone.  In  15  per  cent  the  brain  was  ad- 
herent to  the  membranes  in  the  affected  region  and  in 
17  per  cent  the  brain  substance  between  the  abscess 
and  the  dura  was  softened  and  discolored. 

Abscesses  are  usually  situated  in  the  anterior  por- 
tion of  the  cerebellum.  Those  cases  which  are  sec- 
ondary to  sinus  thrombosis  or  to  epidural  abscess  are 
usually  located  in  the  lateral  hemisphere.  Those 
which  are  secondary  to  labyrinthitis  usually  involve 
the  vermis  or  the  mesial  portion  of  the  lateral  hemi- 
sphere. 

One  of  the  most  interesting  problems  connected 
with  the  pathology  of  brain  abscess  in  general,  but 
particularly  with  cerebellar  abscess  is  that  concerning 
the  process  by  which  the  brain  substance  itself  be- 
comes infected. 

Cerebellar  abscesses  may  be  divided  into  two  classes 
viz. :  superficial  and  deep.  The  former  are  situated  in 


ETIOLOGY  AND  PATHOLOGY        89 

the  cortex  of  the  cerebelkim  and  the  latter  in  the  cen- 
tral white  substance.  The  pathogenesis  of  these  two 
forms  is  entirely  different. 

The  superficial  abscesses  are  formed  as  follows :  the 
purulent  process  in  the  temporal  bone  passes  into  the 
posterior  fossa,  forming  an  epidural  abscess.  There 
follows  an  extension  of  the  inflammatory  process 
through  the  dura  with  the  formation  of  adhesions  be- 
tween the  dura,  pia-arachnoid  and  surface  of  the  cere- 
bellum. The  next  step  is  a  perforation  through  the 
dura  and  the  formation  of  an  abscess  between  the  dura 
and  pia-arachnoid.  This  is  called  a  subdural  abscess. 
The  pia-arachnoid  and  the  superficial  layers  of  the 
cerebellar  cortex  then  break  down  and  suppurate  and 
thus  a  superficial  cerebellar  abscess  results.  This 
type  of  abscess  is  sometimes  called  a  meningo-enceph- 
alitis.  It  is  far  less  common  than  the  second  class 
or  deep  cerebellar  abscess.  All  who  have  observed  a 
number  of  cases  of  brain  abscess  liaA^e  been  impressed 
with  the  fact  that  in  most  instances  the  collection  of 
pus  is  more  or  less  remote  from  the  cortex,  i.  e.,  that 
the  majority  of  brain  abscesses  are  situated  in  the 
white  substance.  To  those  who  have  performed  post- 
mortem examinations  on  a  number  of  these  cases  it 
has  become  evident  that,  between  the  brain  abscess 
and  the  source  of  the  intracranial  infection,  there  is 
frequently  a  layer  of  brain  substance  which  is  macro- 
scopically  normal.    In  other  words  there  is  a  growing 


90  CEREBELLAR  ABSCESS 

impression  that  the  majority  of  brain  abscesses  do 
not  occur  through  direct  extension  by  continuity. 

Even  where  there  is  a  post-petrous  epidural  abscess 
and  where  the  brain  surface  is  grown  fast  to  the  dura 
there  is  often,  interposed  between  the  epidural  abscess 
and  the  brain  abscess,  a  layer  of  normal  brain  tissue. 
Thus  Isemer  in  his  case  report  states:  It  is  remark- 
able that,  although  the  brain  surface  is  grown  fast  to 
the  dura  in  the  region  of  the  epidural  abscess,  yet  be- 
tween the  white  substance  and  the  area  of  the  dura 
there  is  a  distinct,  if  thin,  layer  of  macroscopically  nor- 
mal brain.  From  this  one  might  conclude  that  the 
brain  abscess  was  not  the  result  of  an  extension  by 
continuity  from  the  diseased  labyrinth, ,  but  that  the 
infection  extended  by  thrombosis  of  small  cerebellar 
veins  which  empty  into  the  pial  veins,  or  through  the 
lymph  sheaths  around  these  veins. 

With  regard  to  this  question  Michaelsen  (quoting 
Uffenorde)  states:  The  origin  of  the  brain  infection 
is  always  the  meninges,  i.  e.,  the  dura  and  the  pia- 
arachnoid.  At  first,  the  pial  veins  become  involved 
and  thrombosed.  This  thrombosis  which,  in  the  begin- 
ning, is  not  always  septic,  follows  the  venous  channels 
backwards,  leaving  the  cortex  intact,  until  it  reaches 
the  ultimate  ramifications  of  the  veins  in  the  white 
substance,  where  the  stasis,  producing  red  softening, 
results  in  an  extravasation  of  red  and  white  blood 
cells.    Bacteria  then  pass  into  this  area,  the  brain  tis- 


ETIOLOGY  AXD  PATHOLOGY        91 

sue  breaks  down  and  an  abscess  results.  The  cortex 
is  not  involved  because  of  its  separate  vascular  sys- 
tem. Instead  of  the  veins  being  the  carriers  of  the 
infection,  the  latter  may  travel  along  the  perivascular 
spaces  or  the  lymphatic  vessels.  Sometimes  a  throm- 
bus forms  in  an  artery  and  a  piece  of  this  is  carried 
off  and  lodges  in  a  terminal  vessel  in  some  part  of  the 
cerebellum.  Here  it  causes  necrosis  of  the  brain  tis- 
sue, as  the  cerebral  vessels  are  terminal  vessels.  The 
addition  of  bacteria  in  the  necrotic  area  results  in  the 
formation  of  an  abscess.  A  case  of  this  kind  in  which 
the  abscess  was  located  in  the  frontal  lobe  of  the  brain 
was  seen  by  us  through  the  courtesy  of  Dr.  Berens 
and  reported  by  him  in  the  Annals  of  Otologij,  Bhi- 
noJogy  and  Laryngology,  1914.  As  a  result  of  a 
chronic  middle-ear  suppuration  there  occurred  an  ero- 
sion of  the  internal  carotid  artery  where  it  lies  in  close 
relationship  with  the  inner  w^all  of  the  bony  Eusta- 
chian tube.  An  infected  thrombus  formed  in  the  ar- 
tery. A  portion  of  this  was  washed  away  by  the  blood 
stream  and  lodged  in  a  terminal  vessel  in  the  frontal 
lobe  of  the  brain.  Here  it  caused  an  area  of  necrosis 
with  the  formation  of  a  large  abscess. 

Even  though  the  "origin  of  the  brain  infection  is 
always  the  meninges,"  yet  the  ajDpearance  of  the  dura 
and  its  behavior  during  the  post-operative  treatment 
often  give  absolutely  no  indication  as  to  the  presence 
of  a  brain  abscess.    Collections  of  pus  within  the  brain, 


92  CEREBELLAR  ABSCESS 

with  a  macroscopically  normal  dura  are  not  so  rare. 
In  a  case  of  right  temporo-sphenoidal  abscess  recently 
observed  by  us,  the  dura  was  disclosed  at  operation 
covered  with  cholesteatoma  and  large  pussy  granula- 
tions. During  the  post-operative  dressings  the  dura 
returned  to  normal,  i.  e.,  it  became  coated  with  small 
red  healthy  granulations  and  healing  was  uneventful. 
Two  months  after  the  radical  mastoid  operation  the 
brain  abscess  ruptured  into  the  lateral  ventricle  and 
death  ensued  from  diffuse  purulent  meningitis. 

The  observations  of  Heilbronn,  although  too  iso- 
lated to  be  conclusive  in  themselves,  throw  a  flood 
of  light  upon  the  modus  operandi  of  brain  infection 
through  the  blood  vessels. 

He  states:  "There  are  few  observations  of  brain 
lesions  which  have  occurred  through  venous  channels 
(Riicklaiifigem  Wege).  Such  affections  we  would 
expect  chiefly  in  disease  of  the  great  sinus,  the  chief 
return  current  of  the  brain's  venous  blood.  With  the 
most  frequent  form  of  sinus  disease,  i.  e.,  thrombosis 
and  thrombo-phlebitis,  there  have  been  few  observa- 
tions of  brain  disease.  Oppenheim  in  his  'Lehrbuch 
der  Nervenkrankheiten'  states  that  he  believes  there 
are  many  opportunities  in  cases  of  sinus  thrombosis  to 
observe  focal  brain  symptoms.  Hemorrhage  and  soft- 
ening are  often  the  direct  result  of  sinus  thrombosis, 
and,  althougli  such  observations  are  rare,  they  occur 
far  more  frequently  than  they  are  observed." 


ETIOLOGY  AND  PATHOLOGY        93 

Heilbronn  reports  several  interesting  cases  with 
general  and  focal  brain  symptoms  complicating  otitic 
sinus  thrombosis.  In  the  first  case,  a  patient  with 
acute  suppurative  otitis  media  and  mastoiditis,  sjanp- 
toms  of  meningitis  followed  six  days  after  a  simple 
mastoid  operation  had  been  performed.  With  a  grad- 
ual rise  of  temperature,  the  patient  became  delirious 
and  finally  comatose.  Post-mortem  examination 
show^ed  no  meningitis.  There  was  a  thrombosis  of 
the  left  sigmoid  sinus.  There  were  hemorrhages  in 
both  optic  thalami,  thrombosis  of  the  venee  Galeni  and 
of  other  basal  veins.  The  sjTiiptoms  were  due  to  the 
disturbance  in  the  intracerebral  circulation.  He  draws 
the  following  conclusions: 

1.  In  sinus  thrombosis  bj^  the  plugging  of  the  small 
veins,  lesions  of  the  brain  in  the  form  of  hemorrhages 
and  softening  may  occur. 

2.  These  lesions,  like  many  other  brain  lesions,  may 
cause  general  brain  symptoms  without  definite  focal 
sj-mptoms. 

The  second  case  was  that  of  a  young  man  in  whom 
a  sinus  thrombosis  complicated  a  chronic  suppurative 
otitis  media.  He  suddenly  became  unconscious. 
This  condition,  however,  lasted  but  a  few  hours  and 
was  followed  by  an  aphasia.  Post-mortem  examina- 
tion show^ed  extensive  sinus  thrombosis.  The  laro-e 
pial  vein  which  surrounds  the  left  temporo-sphenoidal 
lobe  and  has  its  origin  in  this  lobe  was  thrombosed. 


94  CEREBELLAR  ABSCESS 

The  aphasia  was  due  to  the  occlusion  of  this  vein 
and  stasis  of  the  blood  with  the  consequent  nutritional 
disturbance.  The  third  case,  probably  the  most  sig- 
nificant, was  that  of  a  young  woman  in  whom  sinus 
thrombosis  complicated  a  chronic  suppurating  ear. 
In  this  instance  there  were  signs  pointing  to  a  bulbar 
lesion.  Anatomically  there  was  no  gross  obstruction 
of  the  veins  leading  from  this  region,  but  in  the 
medulla  there  were  changes  which  doubtless  indicated 
a  destruction  of  function  of  this  part.  There  were 
destruction  of  fibers  and  a  paucity  of  nuclei,  while  the 
remaining  nuclei  stained  poorly  and  were  deformed. 
The  picture  was  one  of  anemic  necrosis.  The  lesions 
were  significantly  distributed  about  the  vessels.  To 
the  center  of  each  focus  ran  a  small  vessel. 

These  observations,  while  they  are,  as  stated,  too 
isolated  to  be  conclusive,  yet  offer  strong  confirmation 
of  Uffenorde's  theory.  Whether  this  theory,  regard- 
ing the  manner  in  which  the  brain  tissue  itself  is 
infected,  holds  good  onh'  for  those  cerebellar  ab- 
scesses which  take  their  origin  in  a  thrombosed  sinus, 
or  whether  it  can  be  applied  to  all  cases  irrespective 
of  their  origin,  remains  to  be  proven.  Only  careful 
histological  research  will  clear  this  point. 

Cerebellar  abscesses  are  usually  irregular  in  shape. 
They  often  have  pockets  or  diverticula,  which  may  be 
connected  with  the  main  abscess  by  means  of  a  narrow 
stalk.     Such  a  diverticulum  may  give  the  impression 


ETIOLOGY  AND  PATHOLOGY        05 

of  a  secondary  abscess,  but  multiple  abscesses  in 
the  cerebellum  are  unusual  except  when  they  are 
pyemic  in  their  origin.  Koerner  found  multiple  ab- 
scesses in  four  cases  out  of  thirty-two  cerebellar 
abscesses. 

The  brain  tissue  sin-rounding  the  abscess  is  actively 
inflamed.  The  vessels  are  hyperemic  and  some  of 
them  are  thrombosed.  Around  the  vessels  are  masses 
of  extravasated  red  and  white  blood  cells.  There  is 
some  edema.  This  encephalitis  causes  an  increase  in 
the  size  of  the  affected  hemisphere  and  pressure  upon 
the  remaining  structures  in  the  posterior  fossa.  The 
vermis,  pons  and  medulla  are  often  pushed  to  one  side 
of  the  median  line.  Pressure  of  the  enlarged  cere- 
bellar hemisphere  upon  the  veins  in  the  posterior  fossa 
may  cause  sufficient  interference  with  the  return  cir- 
culation from  the  pia  lining  the  ventricles  to  cause  an 
internal  hj^drocephalus. 

At  the  periphery  of  the  abscess  the  brain  tissue  is 
necrotic  and  broken  down.  The  surface  of  the  brain 
tissue  directed  toward  the  abscess  cavitj^  is  ragged. 
Thrombosed  vessels  project  into  the  cavity.  The 
thrombosis  in  the  vessels  at  the  periphery  of  the  ab- 
scess prevents  bleeding  ir^to  the  cavity.  When  the 
breaking  down  of  tissue  is  more  rapid  than  the  throm- 
bus formation  hemorrhage  occurs. 

When  the  breaking  down  of  the  tissue  has  ceased 
and  the  brain  tissue  has  sufficient  vitalitv  to  manifest 


96  cp:rebellar  abscess 

a  tendency  to  reparative  processes,  a  network  of  fibrin 
is  formed  at  the  periphery  of  the  abscess.  This  fibrin 
network  is  formed  from  the  elements  of  the  surround- 
ing hving  tissue.  Leucocytes  pass  into  this  network, 
gradually  become  spindle-shaped  and  finally  change 
to  connective-tissue  cells.  In  this  way  a  capsule  is 
formed  about  the  abscess.  At  first  the  capsule  is  non- 
vascular. Later,  primitive  blood  vessels  pass  into  the 
capsule  from  the  periphery.  The  membrane  gradually 
becomes  thicker  and  separates  the  abscess  from  the 
normal  brain  tissue.  The  growth  of  the  abscess  is  usu- 
ally slower  after  the  capsule  has  formed,  and  may 
cease  altogether.  The  capsule  may  be  from  1  to  5  mm. 
or  more  in  thickness.  The  older  the  abscess,  the  thicker 
the  capsule,  as  a  rule.  A  capsule  has  been  found  in 
abscesses  which  were  only  five  or  six  weeks  old.  Some- 
times the  periphery  of  the  capsule  becomes  very  dense 
and  fibrous  with  very  few  blood  vessels,  or  it  may 
even  become  calcified. 

The  histological  appearance  of  a  typical  abscess 
capsule  is  described  by  Oppenheim  as  follows :  "Three 
zones  are  seen  in  the  capsule.  The  inner  gi-anulation 
zone  shows  no  sharp  demarkation  from  the  abscess 
cavity.  It  consists  of  numerous  roimd  cells  with  very 
little  intercellular  substance  and  very  few  vessels.  The 
second  zone  consists  partly  of  wavy  and  partly  of 
straight  fibers.  In  the  central  portion  of  this  zone 
the  fibers  are  closely  packed  and  in  the  peripheral  por- 


ETIOLOGY  AND  PATHOLOGY        97 

tion,  more  loosely  arranged.  Between  the  fibers,  in 
addition  to  spindle  cells,  there  are  cells  which  repre- 
sent partially  changed  glia  cells  and  round  cells.  In 
this  layer  there  are  numerous  thick-walled  blood  ves- 
sels. The  fibroblasts  which  form  the  fibrous  tissue, 
seem  to  belong  only  to  the  mesodermal  tissue  (vessel 
walls  and  connective  tissue  surrounding  the  vessel 
walls ) ,  whereas  the  neuroglia  seems  to  take  no  part  in 
this  formation.  The  third  or  outer  zone  consists  of 
a  more  uniform  ground  substance  which  contains 
numerous  round  cells  and  large  swollen  glia  cells.  In 
no  place  is  there  a  sharp  demarkation  between  the 
healthy  tissue  and  the  capsule.  Everywhere  there  are 
signs  of  an  active  process  and  nowhere  is  there  real 
cicatrization." 

Not  all  brain  abscesses  have  capsules.  The  pres- 
ence of  a  capsule  does  not  prevent  an  increase  in  the 
size  of  the  abscess.  The  capsule  may  be  replaced  by 
exuberant  granulations,  pus  may  be  formed  anew, 
and  thus  the  abscess  may  enlarge.  The  capsule 
stretches  and  may  finally  rupture,  the  abscess  empty- 
ing itself  into  the  fourth  ventricle  or  the  subarachnoid 
space. 

An  encapsulated  abscess  sometimes  acts  as  a  for- 
eign body  and  sets  up  irritative  changes  in  the  sur- 
rounding tissue.  Thus  a  second  abscess  may  be 
formed  in  which  the  first  encapsulated  abscess  is 
found  floating.    Encapsulated  abscesses  may  remain 


98  CEREBELLAR  ABSCESS 

latent  for  a  long  time,  sometimes  several  years,  and 
then  enlarge  and  rupture. 

When  a  fistula  from  the  mastoid  communicates 
with  the  interior  of  the  cerebellar  abscess,  it  is  not  the 
result  of  a  breaking  down  of  tissue  from  the  surface 
to  the  interior  of  the  abscess.  The  abscess  ruptures 
onto  the  surface  of  the  cerebelkim,  forming  first  a  sub- 
dural abscess,  and  then  perforating  through  the  dura 
into  the  mastoid  cavity. 

Around  the  abscess,  the  brain  tissue  is  always  more 
or  less  inflamed.  This  encephalitic  area  may  be  very 
extensive.  The  encephalitis  may  extend  and  cause 
death  even  after  the  abscess  has  been  evacuated.  It 
manifests  itself  macroscopically,  on  cross-section  of 
the  brain,  by  swelling  of  the  brain  tissue  and  by  fine 
red  dots  resembling  flea-bites,  scattered  through  the 
white  matter.  In  a  histological  examination  of  such 
an  encephalitic  area,  Dupre  and  Deveaux  found  dif- 
fuse degeneration  of  the  cortical  cells  without  involve- 
ment of  the  nerve  fibers.  They  concluded  that  these 
changes  are  due  to  toxins  which  arise  from  the 
abscess. 

The  contents  of  the  abscess  consist  of  pus  cells, 
many  of  which  are  undergoing  fatty  changes,  large 
mononuclear  lymphocytes,  red  blood  cells  and  free 
nuclei.  Between  the  cells  is  an  amorphous  exudate, 
fragments  of  dead  tissue,  hematoidin,  margarin  and 
cholesterin  crystals  and  bacteria. 


ETIOLOC:^Y  AND  PATHOLOGY        99 

Many  kinds  of  bacteria  have  been  found  in  cere- 
bellar abscess.  Streptococcus  pyogenes  and  staphylo- 
coccus pyogenes  aureus  are  the  most  common. 
Staphylococcus  pyogenes  albus  and  citreus  are  less 
common.  Streptococcus  mucosus  capsulatus,  pneu- 
mococcus  and  bacillus  of  Friedlaender  occur.  The 
same  organisms  may  be  found  in  the  abscess  as  occur 
in  the  middle-ear  suppurations.  Bacillus  pyocyaneus, 
streptococcus  pyogenes  fetidus,  micrococcus  pyogenes 
tenuis,  bacillus  typhosus,  bacterium  coli  and  bacillus 
proteus  vulgaris  have  been  found. 

Mixed  infections  often  occur.  Saprophytic  organ- 
isms are  sometimes  found  together  with  pyogenic  or- 
ganisms. Occasionally  saprophytic  organisms  are 
found  alone.  When  this  occurs,  it  is  probable  that 
pyogenic  organisms  were  present,  but  have  died  out. 
Occasionally  no  bacteria  are  found  in  the  abscess. 
Tubercle  bacilli  have  been  found. 

According  to  Neumann,  when  the  abscess  is  due  to 
diplococci,  fibrinoplastic  changes  occur,  which  result 
in  well-marked  demarkation  and  encapsulation. 
When  it  is  due  to  anaerobic  bacteria,  there  are  soft 
necrotic  margins  and  no  attempt  at  encapsulation. 
The  anaerobes  produce  sulphuretted  hydrogen,  which 
gives  the  fetid  odor  to  some  brain  abscesses.  These 
anaerobic  bacteria  flourish  in  the  mouth  as  harmless 
saprophytes  and  pass  into  the  middle-ear  through  the 
Eustachian  tube. 


100  CEREBELLAR  ABSCESS 

In  some  cases,  different  organisms  were  found  in 
the  middle-ear,  brain  abscess  and  spinal  fluid.  In  the 
same  abscess  different  bacteria  Mere  found  at  different 
times. 

In  acute  abscesses,  the  cavity  of  the  abscess  becomes 
obliterated  as  soon  as  it  is  evacuated,  as  a  result  of  the 
pressure  of  the  surrounding  swollen  brain  tissue.  In 
chronic  abscesses,  with  rigid  walls,  it  may  take  many 
weeks  before  the  abscess  cavity  is  obliterated. 

The  cases  of  brain  abscess  which  evacuate  them- 
selves spontaneously,  through  a  fistula  into  the  mas- 
toid, and  thence  through  a  perforation  in  the  drum- 
membrane,  or  through  a  fistula  in  the  skin  over  the 
mastoid,  do  not  heal,  as  the  fistula  is  so  narrow  and 
tortuous  that  it  does  not  provide  adequate  drainage. 

Very  rarely,  according  to  Macewen,  a  brain  ab- 
scess may  heal  spontaneously  and  become  absorbed. 
Blood  vessels  from  the  normal  brain  tissue  may  pene- 
trate the  abscess  capsule  and  cause  resorption  of  the 
pus  through  phagocytosis. 


CHAPTER  IV 

SYMPTOMS  OF  CEREBELLAR  ABSCESS 


CHAPTER  IV 

SYMPTOMS    OF    CEREBELLAR   ABSCESS 

THE  symptoms  of  cerebellar  abscess  divide 
themselves  into  two  groups.  In  the  first 
group  must  be  placed  those  symptoms  which 
are  common  to  all  forms  of  intracranial  compli- 
cations. The  second  group  consists  of  those  phe- 
nomena which  are  peculiar  to  cerebellar  lesions  and 
are  the  result  of  disturbance  in  cerebellar  func- 
tion. Lesions  of  the  fiber  tracts  in  the  cerebellum 
w^hich  connect  the  vestibular  nuclei  with  the  cerebellar 
nuclei  and  the  cerebellar  cortex  give  rise  to  symptoms 
similar  to  those  caused  by  lesions  of  the  vestibular 
centers  or  of  the  static  labyrinth.  Consequently  the 
focal  symptoms  of  cerebellar  abscess  may  be  divided 
into  two  groups. 

A.  SjTnptoms  of  disturbances  in  movements. 

B.  Symptoms    of   disturbances   in   the   vestibular 
apparatus. 

A.  The  symptoms  of  disturbance  of  movement  are 
the  following: 

1.  Hypermetria. 

2.  Asynergy. 

3.  Adiadokokinesis. 

103 


104  CEREBELLAR  ABSCESS 

4.  Tremor. 

5.  Disturbances  in  writing. 

6.  Disturbances  in  speech. 

7.  Atony  or  hypotony. 

8.  Catalepsy. 

9.  Spontaneous  deviations  of  the  extremities 

and  loss  of  reaction  movements. 

10.  Spontaneous  falling  and  loss  of  reaction 
movements  of  the  trunk. 

11.  Hemiparesis. 

12.  Fixed  attitude  of  the  head. 

13.  Disturbances  in  weight  estimation. 

B.  The  symptoms  which  are  due  to  destruction  of 
the  fiber  tracts  between  the  vestibular  nuclei  and  the 
cerebellar  nuclei  are: 

1.  Nystagmus. 

2.  Enduring  nystagmus. 

3.  Vertigo. 

4.  Vomiting. 

The  general  sjniiptoms  of  cerebellar  abscess  may  be 
divided  into  two  groups. 

A.  Those  due  to  increased  intracranial  pressure. 

B.  Those  due  to  the  inflammatory  process  in  the 
cerebellum. 

A.  Symptoms  due  to  increase  in  intracranial  pres- 
sure are: 

1.  Headache. 

2.  Vomiting. 


SYMPTOMS  105 

3.  Disturbances  of  the  sensorium. 

4.  Slow  pulse. 

5.  Disturbances  of  respiration. 

6.  Optic  nerve  changes. 

7.  Paralysis  of  the  cranial  nerves. 

8.  Changes  in  the  reflexes. 

B.  The  symptoms  due  to  the  inflammatory  process 
in  the  cerebellum  are: 

1.  Changes  in  temperature. 

2.  Emaciation. 

3.  Changes  in  the  blood. 

4.  Changes  in  the  cerebrospinal  fluid. 
Headache  is  the  most  constant  of  the  symptoms  of 

cerebellar  abscess.  It  was  mentioned  in  70  cases 
out  of  the  86  collected.  It  is  usually  intermittent  as 
are  most  of  the  general  symptoms.  Occasionally 
the  headache  is  dull  and  boring  with  exacerba- 
tions which  are  unbearably  severe.  There  may  be 
periods  during  which  the  patient  is  entirely  free  from 
pain.  The  location  of  the  headache  is  not  character- 
istic but  it  is  most  commonly  occipital.  Sometimes 
there  is  tenderness  to  percussion  of  the  skull  over  the 
site  of  the  abscess. 

Vomiting  is  more  persistent  with  cerebellar  ab- 
scess than  with  abscess  in  the  temporo-sphenoidal 
lobe.  It  was  mentioned  in  48  out  of  the  86  cases.  It 
may  occur  with  or  without  nausea.  There  are  two 
types  of  vomiting  with  cerebellar  abscess,  viz.,  projec- 


106  CEREBELLAR  ABSCESS 

tile,  which  is  due  to  tlie  increased  intracranial  pressure 
and  vomiting  accompanied  by  nausea,  which  is  due  to 
involvement  of  the  vestibulo-cerebellar  tracts.  The 
vomiting  bears  no  relationship  to  the  ingestion  of 
food.  Nausea  without  vomiting  was  mentioned  in 
four  cases. 

Mental  dulness  and  somnolence  are  rarer  with  cere- 
bellar abscess  than  with  cerebral  abscess.  In  all  prob- 
ability the  mental  changes  are  toxic  in  origin  and  are 
not  due  to  pressure.  Drowsiness  was  noted  in  32  of 
the  cases.    Delirium  or  hyperexcitability  is  rare. 

Bradycardia  is  a  sjmiptom  frequently  met  with  in 
cerebellar  abscess.  It  was  mentioned  in  38  of  the 
cases.  The  pulse  is  not  uniformly  slow  during  the 
entire  24  hours.  While  during  most  of  the  day,  it 
may  range  between  60  and  75,  for  a  short  time  it 
may  drop  to  50  or  even  lower.  This  drop  often  oc- 
curs during  the  early  morning  hours.  The  pulse  is 
always  slow  in  relation  to  the  temperature,  so  that 
even  with  a  complicating  meningitis  and  a  tempera- 
ture of  103°  F.  or  104°  F.,  the  pulse  is  not  hkely  to 
be  above  70. 

Pressure  of  the  abscess  on  the  medulla  sometimes 
causes  disturbances  of  respiration.  Respiration  may 
be  as  low  as  10  or  12  to  the  minute.  It  may  take  on 
the  Cheyne- Stokes  type.  In  a  number  of  cases  res- 
piration suddenly  ceased  during  operation  for  cere- 
bellar abscess  while  the  heart  continued  to  beat. 


SYMPTOMS  107 

Optic  nerve  changes  were  present  in  16  of  the 
cases.  The  condition  found  is  usually  an  optic  neu- 
ritis but  occasionally  there  is  choked  disc.  It  may  be 
unilateral  or  bilateral,  and  if  unilateral,  may  be  on 
the  affected  side  or  on  the  opposite  side.  The  impair- 
ment of  vision  is  usually  not  very  great.  Oi^tic  nerve 
changes  occur  a  great  deal  more  frequently  in  cere- 
bellar abscess  than  in  abscess  of  the  temporo-sphe- 
noidal  lobe. 

Paralyses  of  the  third,  fifth,  or  sixth  nerves  were 
present  eleven  times.  Inequality  of  the  pupils  was 
present  in  four  of  the  cases,  and  in  two  the  pupils 
were  dilated  and  unequal.  Anesthesia  of  the  cornea 
occasional!}^  occurs.  These  paralyses  are  due  either 
to  an  accompanying  basilar  meningitis  or  to  pressure 
upon  the  nerves.  In  some  cases  there  is  present,  in- 
stead of  a  third  or  sixth  nerve  paralysis  on  one  side, 
a  conjugate  deviation  of  the  eyes.  This  may  be 
accompanied  by  a  deviation  of  the  head.  Facial 
paralysis  or  paresis  occurred  in  27  cases.  In  the 
majority  of  these,  the  paralysis  was  due  to  in- 
volvement of  the  facial  nerve  in  the  temporal  bone, 
as  the  result  of  the  accompanying  labyrinthine  suppu- 
ration. In  a  few  cases  it  was  due  to  pressure  on  the 
intracranial  portion  of  the  nerve.  The  difficulty  in 
swallowing,  which  occurs  occasionally,  may  be  due 
either  to  pressure  on  the  glossopharyngeal  nerve  or  to 
pressure  on  the  medulla.      Changes  in  the  reflexes 


108  CEREBELLAR  ABSCESS 

were  mentioned  in  7  cases  out  of  the  86.  They  were 
increased  in  5  and  diminished  in  2. 

The  temperature  was  noted  in  55  of  the  cases. 
It  was  above  100°  F.  in  23.  It  was  between  98.6° 
F.  and  100°  F.  in  21  cases.  It  was  subnormal  in  11 
cases.  The  higher  temperatures  usually  occur  in  the 
terminal  stages  after  a  meningitis  has  set  in.  A  per- 
sistently normal  temperature  does  not  exclude  cerebel- 
lar abscess. 

Partly,  perhaps,  because  of  the  persistent  vomit- 
ing, but  much  more  because  of  the  profound  trophic 
disturbance,  cerebellar  abscess  causes  a  rapid  and  ex- 
treme emaciation.  The  patients  are  cachectic  in 
appearance.  They  are  usually  constipated,  with 
coated  tongue  and  fetid  breath.  There  is  rarely  any 
bladder  disturbance  except  just  before  death. 

The  blood  changes  with  cerebellar  abscess  are 
not  characteristic.  There  may  be  a  leucocytosis 
with  a  high  polynuclear  count,  or  the  blood  picture 
may  be  normal.  No  cases  of  bacteriemia  have  been 
reported  in  uncomplicated  cases  of  cerebellar  ab- 
scess. 

The  cerebrospinal  fluid  was  examined  in  24  of  the 
cases.  It  was  normal  in  9  of  the  cases ;  it  was  normal 
but  under  increased  pressure  in  2  cases ;  it  was  cloudy 
and  sterile  in  8  cases.  In  3  of  these  the  fluid  was  un- 
der increased  pressure.  It  contained  bacteria  in  5 
cases.     In  our  own  experience  a  cloudy,  sterile  fluid 


SYMPTOMS  109 

was  the  most  common  finding  in  uncomplicated  brain 
abscess. 

The  focal  symptoms  of  cerebellar  abscess  are  due  to, 

1.  Destruction  of  brain  tissue. 

2.  The  encephalitis  surrounding  the  abscess. 

3.  Pressure  of  the  abscess  on  the  surrounding  tis- 
sues. 

The  symptoms  due  to  actual  destruction  of  brain 
tissue  are  permanent.  Those  due  to  encephalitis  and 
pressure  may  disappear  after  the  abscess  is  evacuated. 

The  symptoms  of  disturbance  of  movement  are  the 
following : 

1.  Hypermetria. — The  cerebellum  seems  to  exercise 
an  inhibitory  influence  on  movements.  In  cerebellar 
lesions,  there  is  a  suppression  of  this  inhibition,  result- 
ing in  unmeasured  or  immoderate  movements.  This 
is  called  hj^permetria.  It  may  occur  in  spontaneous 
movements,  but  is  much  more  likely  to  occur  in  cer- 
tain commanded  movements.  For  instance,  if  a  pa- 
tient with  cerebellar  abscess  is  asked  to  touch  the  tip 
of  his  nose  with  the  end  of  his  index  finger  he  will 
point  past  the  nose.  A  similar  hypermetria  due  to 
overflexion  of  the  thigh  may  be  observed  when  a 
patient  attempts  to  touch  the  knee  with  the  opposite 
heel. 

If  a  patient  is  seated,  with  the  palm  of  his  hand  on 
the  knee  of  the  same  side,  and  he  is  asked  to  supinate 
the  hand  so  that  the  back  of  his  hand  rests  on  the  same 


110  CEREBELLAR  ABSCESS 

s^Dot  ^\here  the  palm  was,  the  movement  will  be  over- 
done, and  the  ulnar  side  of  the  hand  will  lie  higher 
than  the  radial. 

A  vertical  line  is  drawn  near  the  right  edge  of  a 
sheet  of  paper.  The  patient  is  asked  to  draw  hori- 
zontal lines,  starting  anywhere,  but  ending  at  the  ver- 
tical line.  The  patient  will  continue  all  of  his  lines 
past  the  vertical  line. 

In  walking,  at  the  beginning  of  the  step,  flexion 
of  the  thigh  on  the  pelvis  is  more  pronounced  than 
normal,  leading  to  excessive  raising  of  the  foot.  At 
the  end  of  the  step,  the  sole  of  the  foot  makes  a  greater 
noise  than  normal  in  striking  the  floor,  denoting 
excessive  extension  of  the  thigh. 

The  hypermetria  is  best  brought  out  if  the  patient 
is  asked  to  perform  the  movement  quickly,  for,  if  it 
is  done  slowly,  he  can  correct  the  error. 

Vision  has  no  effect  on  the  movements.  The  same 
error  is  made  with  the  eyes  open,  as  with  the  eyes 
closed. 

The  direction  of  the  movement  is  conserved.  It 
passes  the  mark,  and  then  deviates. 

2.  Cerebellar  Asynergy. — If  a  patient  with  cere- 
bellar abscess  is  supported  on  either  side,  without  his 
movements  being  influenced,  and  asked  to  walk,  he 
will  stop  at  his  first  step.  The  thigh  is  flexed  and  the 
foot  is  carried  forward,  but  the  upper  part  of  the 
body  does  not  move  in  harmony  with  the  legs,  the 


SYMPTOMS  111 

trunk  remaining  extended  on  the  thighs.  Thus,  hav- 
ing placed  his  foot  on  the  ground  with  much  noise, 
at  the  end  of  his  first  step,  he  can  go  no  further.  He 
is  in  danger  of  falling  hackward.  It  is  necessary  for 
the  assistant  to  push  the  upper  part  of  the  body  for- 
ward, or  the  patient  can  help  himself  by  pulling  his 
trunk  forward  with  his  arms,  his  hands  catching  some 
support  in  front  of  him. 

If  a  patient,  standing  up,  is  asked  to  bend  his  head 
back  and  curve  his  body  backward,  he  falls,  because 
he  only  bends  the  trunk  back,  without  bending  the 
legs  on  the  feet  and  the  thighs  on  the  legs. 

If  a  patient  with  a  cerebellar  lesion  lies  on  his 
back,  with  his  arms  crossed  on  his  breast,  he  cannot 
sit  up.  He  flexes  the  thighs  at  the  hip,  and  lifts  the 
heels  from  the  floor. 

These  tests  show  that  a  patient  w4th  cerebellar 
abscess  cannot  synchronize  the  movements  at  the  vari- 
ous joints  in  such  a  way  as  to  perform  an  effective 
complex  movement.  Closing  the  eyes  does  not  change 
this. 

3.  Adiadokokmesis. — This  is  the  abolition  or  the 
diminution  of  the  faculty  of  executing  rapidly  succes- 
sive voluntary  movements. 

In  a  cerebellar  lesion,  muscular  force  is  intact.  The 
patient  can  execute  as  rapidly  as  a  normal  individual 
the  elementary  movements,  pronation  or  supination. 
But  the  complete  movement  (pronation  and  supina- 


112  CEREBELLAR  ABSCESS   ' 

tion)  he  performs  more  sloM^y  than  a  normal  indi- 
vidual. The  phenomenon  becomes  more  manifest  if 
the  act  is  repeated  a  number  of  times. 

The  symptom  is  present  only  in  an  individual  who 
can  perform  the  isolated  movement,  pronation  or  supi- 
nation, with  normal  rapidity.  For  if  he  cannot  do 
this,  he  cannot,  of  course,  perform  a  rapid  succession 
of  the  two  movements. 

It  is  sometimes  bilateral,  and  sometimes  unilateral. 
In  the  latter  case,  it  occurs  on  the  same  side  as  the 
cerebellar  lesion. 

4.  Tremor. — On  attempting  to  point  to  an  object 
with  one  of  the  extremities,  orientation  is  correct,  but 
the  movement  is  not  uniform.  There  are  oscillations 
in  different  directions.  The  tremor  occurs  only  dur- 
ing voluntary  contraction  of  the  muscles.  It  varies 
in  different  individuals,  and  in  the  same  individual  at 
different  times.  It  maj^  diminish,  if  the  patient  is  left 
to  himself,  and  not  observed,  and  if  he  executes  move- 
ments slowly  and  carefully. 

On  pointing  to  the  nose  with  the  finger,  the  move- 
ment to  the  nose  may  be  direct,  and  then,  at  the  end, 
there  may  be  violent  tremor. 

5.  Disturbances  in  Writing. — If  one  ask  a  patient 
with  a  cerebellar  lesion  to  make  a  dot  with  a  pencil, 
on  a  sheet  of  paper,  he  rarely  succeeds  at  the  first 
attempt.  At  first  he  either  breaks  the  point  or  forces 
it  through  the  paper.    At  the  second  attempt,  he  stops 


SYMPTOMS  113 

above  the  paper.  Finally,  finding  the  surface  of  the 
paper,  he  makes,  not  a  dot,  but  a  line. 

Cerebellar  patients  place  commas  and  not  dots  over 
their  i's.  This  is  hypermetria.  If  they  are  asked  to 
draw  a  line  of  a  certain  length,  they  will  extend  it 
further. 

In  attempting  to  draw  a  circle  or  an  arc,  as  in  the 
letters  O  or  C,  the  figin-e  is  potygonal. 

In  attempting  to  reproduce  regular  zigzags,  as  in 
m  and  n,  the  angles  are  badly  formed,  and  the  lines 
irregular.  Having  arrived  at  the  end  of  a  line,  the 
patient  finds  it  difficult  to  begin  a  new  line  in  the 
opposite  direction. 

The  irregularities  in  writing  are  the  result  of 
tremor,  hypermetria,  asynergy  and  adiadokokinesis. 

6.  TJisturhances  of  Speech. — ^Speech  is  scanning, 
jerky,  a  little  explosive,  and  sometimes  dragging.  It 
is  similar  to  that  in  disseminate  sclerosis. 

7.  Atony  or  Hypotony. — Hypotony  is  present  in 
a  few  cases.  It  is  sometimes  bilateral  and  sometimes 
unilateral,  in  which  case  it  is  on  the  side  of  the  lesion. 
An  experiment  for  determining  the  presence  of 
hypotony  of  the  extensors  of  the  arm  is  as  follows: 
Ask  the  patient  to  flex  the  forearm,  and  oppose  this 
by  traction  on  his  forearm.  Suddenly  stop  the  trac- 
tion. In  a  normal  person,  there  results  pronounced 
flexion,  followed  by  a  violent  extension.  In  cerebellar 
lesions,  this  extension  is  only  indicated. 


114  CEREBELLAR  ABSCESS 

8.  Cerebellar  Catalepsy. — This  is  a  rare  symptom. 
In  certain  positions  where  volitional  equilibrium  is  re- 
alized, the  voluntary  muscles  are  held  immobile  for 
a  long  time  without  being  contracted.  It  often  ap- 
pears as  follows :  The  patient  lies  on  his  back,  thighs 
flexed  on  pelvis,  legs  lightly  flexed  on  thighs,  feet  sep- 
arated. When  he  assumes  this  attitude,  his  legs  and 
trunk  oscillate  in  various  directions,  especially  from 
left  to  right  and  vice  versa,  but  at  the  end  of  several 
seconds,  the  body  and  lower  limbs  become  fixed.  This 
fixity  is  more  marked  than  a  normal  individual  can 
attain.  It  persists  for  several  minutes,  and  causes 
no  sensation  of  fatigue. 

In  cerebellar  affections,  volitional  kinetic  equilib- 
rium is  diminished,  while  volitional  static  equilibrium 
is  preserved  or  even  increased. 

9.  Simntaneous  Deviation  of  the  ELVtremities,  and 
Loss  of  Reaction  Movements. — These  symptoms,  as 
worked  out  by  Barany,  are  of  extreme  importance  in 
the  diagnosis  of  cerebellar  abscess.      (Figs.  15-20.) 

The  method  of  examination  is  as  follows:  The 
patient  is  seated  with  his  eyes  closed.  His  arm  is  ex- 
tended before  him,  and  the  index  finger  is  made  to 
touch  the  palmar  surface  of  the  examiner's  index 
finger.  The  arm  is  then  lowered  until  the  hand 
touches  the  knee,  and  then  raised  until  the  finger  again 
touches  the  examiner's  finger,  which,  meanwhile,  has 
not  been  moved.      With  a  normal  cerebellum,  the 


Fig.   15. — Pointing  Test  for  Rotation. 
115 


Fig.   16. — Loss  of  Pointing  Reaction  after  Rotation. 

117 


Fig.    17. — Normal   Pointing  Reaction   after   Rotation   to 

Left. 

119 


YiG,   18. — Pointing   Reaction    with    C  alohk    Vestiuular 

Stimulation. 

121 


Fig.    19- — Pointing   Reaction    at    Klijow   Joint. 
123 


Fig.  20. — Pointing  Reaction   at  Whist  Joint. 
125 


SYMPTOMS  127 

patient  points  correctly.  With  a  lesion  in  the  shoul- 
der area  of  the  cerebellar  cortex,  the  arm  will 
deviate  either  inward  or  outward.  If  the  lesion  is 
in  the  right  biventral  lobe,  the  right  arm  will  deviate 
outward,  or  to  the  right.  If  the  lesion  is  at  the  middle 
of  the  margin  of  the  right  cerebellar  hemisphere,  i.  e., 
at  the  middle  of  the  right  postero-superior  and  pos- 
tero-inferior  lobes,  the  right  arm  will  deviate  inward, 
or  to  the  left.  The  former  area  contains  the  center  for 
inward  tonus  of  the  shoulder  joint  and  the  latter  the 
center  for  outward  tonus  of  the  shoulder  joint.  The 
left  arm  will  point  correctly.  The  deviation  involves 
only  the  side  of  the  body  on  which  the  lesion  occurs. 
The  movements  of  the  elbow  joint  are  examined  by 
resting  the  elbow  on  the  back  of  a  chair,  and  moving 
the  forearm.  The  movements  of  the  wrist  joint  are 
examined  by  resting  the  wrist  on  the  back  of  a  chair, 
and  moving  the  hand  at  the  wrist.  The  wrist  joint  is 
examined  with  the  hand  in  pronation,  and  then  with 
the  hand  in  supination,  there  being  a  separate  center 
for  each  position  of  the  hand.  The  wrist  center  lies 
in  front  of  the  arm  center. 

The  hip  is  examined  in  a  similar  way.  The  hip 
center  is  behind  the  arm  center.  These  tests  should 
be  made  repeatedly  in  order  to  make  sure  that  there 
really  is  a  deviation,  and  the  patient  must  not  know 
when  he  has  made  an  error  in  pointing  as  he  will  then 
make  an  effort  to  correct  the  error. 


128  CEREBELLAR  ABSCESS 

When  the  lesion  in  the  cortex  is  a  large  one,  many 
joints  will  be  involved  in  the  deviation.  When  the 
lesion  is  small,  only  one  or  two  joints  will  be  involved. 

Having  determined  the  presence  of  a  spontaneous 
deviation,  the  next  step  is  to  test  the  reaction  move- 
ments of  the  extremities.  This  is  done  by  arousing 
a  vestibular  impulse. 

If  the  patient  is  rotated  to  the  left,  he  will  have  an 
after-nystagmus  to  the  right.  If  the  patient's  arms 
are  now  held  in  front  of  him,  they  will  both  deviate 
to  the  left,  i.  e.,  in  the  direction  of  the  slow  component 
of  the  nystagmus,  provided  the  cerebellum  is  normal. 
If,  however,  the  patient  has  a  lesion  in  the  right  cere- 
bellar cortex  involving  the  center  for  inward  tonus  of 
the  shoulder  joint,  the  right  arm  will  point  correctly, 
while  the  left  arm  will  deviate  to  the  left. 

Therefore  with  destruction  of  this  center,  there  is  a 
spontaneous  deviation  of  the  arm  outward,  and  a  loss 
of  the  reaction  movement  inward. 

Instead  of  rotation,  the  caloric  test  may  be  used  to 
arouse  the  reaction  movements,  the  head  being  tilted 
back  60°,  in  order  to  elicit  a  horizontal  nystagmus. 
If  a  cold  caloric  is  done  in  the  left  ear,  and  the  head 
held  upright,  the  arms  held  in  front  of  the  body  will 
deviate  to  the  left.  If  the  right  arm  is  moved  later- 
ally, it  will  deviate  upward.  If  the  left  arm  be  moved 
laterally,  it  will  deviate  downward. 

If  the  head  is  now  rotated  to  the  right  shoulder. 


SYMPTOMS  129 

both  arms  held  in  front  of  the  body  will  deviate  down- 
ward. If  the  head  is  rotated  to  the  left  shoulder,  both 
arms  held  in  front  of  the  body  will  deviate  upward. 

The  deviation  depends  upon  the  plane  and  direction 
of  the  m^stagmus,  and  the  position  of  the  head.  It 
is  always  in  the  plane  of  the  nystagmus,  and  in  the 
direction  of  the  slow  component  of  the  latter. 

10.  Spontaneous  Falling,  and  Reaction  Movements 
of  the  Trunk. — With  an  abscess  involving  the  worm, 
there  is  a  tendency  to  fall.  The  falling  may  be  in 
any  direction.  The  direction  of  falling  was  noted  in 
13  out  of  the  86  cases  collected.  Of  these,  10  cases 
fell  to  the  side  of  the  lesion,  and  3  cases  to  the  oppo- 
site side.  If  spontaneous  m^stagmus  is  present,  the  di- 
rection of  the  falling  does  not  bear  any  definite  rela- 
tion to  this  nystagmus. 

If  an  artificial  rotatory  nystagmus  is  aroused  by 
means  of  cold  or  hot  water  in  the  ear,  the  patient  falls 
in  the  direction  of  the  slow  component  of  the  nystag- 
mus, when  the  vermis  is  intact.  For  instance,  if  cold 
water  is  allowed  to  flow  into  the  right  ear,  the  patient 
falls  to  the  right.  If  the  head  is  turned  to  the  left 
shoulder,  the  patient  falls  forward.  However,  if  there 
is  a  lesion  of  the  vermis,  and  the  patient  falls,  for 
example,  backward,  the  direction  of  the  falling  would 
not  be  changed  by  the  production  of  a  caloric  vestibu- 
lar impulse.  In  other  words,  the  falling  reaction  is 
wanting.     There  may  be  an  absence  of  the  falling 


130  CEREBELLAR  ABSCESS 

reaction  without  spontaneous  falling.  The  loss  of  the 
falling  reaction  may  be  in  one  or  several  directions. 
In  the  latter  case,  the  lesion  would  be  larger  and  more 
centrally  located  than  in  the  former. 

In  order  to  differentiate  between  focal  lesions  and 
symptoms  due  to  pressure  from  a  distance,  we  must 
make  a  careful  examination  of  the  spontaneous  symp- 
toms as  well  as  a  careful  functional  examination.  If 
there  is  spontaneous  falling  or  deviation  of  the  extrem- 
ities, and  on  arousing  the  proper  vestibular  impulse,  a 
falling  or  deviation  in  the  opposite  direction  is  elicited, 
we  are  dealing  with  a  distant  lesion.  If,  on  examina- 
tion at  different  times,  there  is  sometimes  deviation 
and  falling  and  sometimes  none,  we  are  surely  deal- 
ing with  a  distant  lesion.  If  only  a  portion  of  the 
sjTnptoms  change,  there  is  a  combination  of  focal 
lesion  and  lesion  at  a  distance.  If,  after  a  decompres- 
sion operation,  the  symptoms  disappear,  there  is  a 
lesion  at  a  distance. 

Constant  symptoms  which  increase  in  severity  are 
due  to  focal  lesions. 

11.  Hemiparesis. — This  symptom  occurs  occa- 
sionally in  cases  of  cerebellar  abscess.  It  was 
noted  in  6  cases  out  of  the  86  collected  from  the 
literature.  It  is  always  on  the  same  side  as  the  cere- 
bellar lesion. 

12.  Fixed  Attitude  of  the  Head. — In  a  few  cases  of 
cerebellar  abscess,  the  head  is  held  stiff  and  rigid,  and 


SYMPTOMS  131 

bent  toward  one  shoulder.  The  cause  of  this  attitude 
is  not  definitely  known.  It  may  be  due  to  increased 
tonus  of  the  neck  muscles  of  one  side.  In  experiments 
on  dogs,  where  half  of  the  cerebellum  is  removed,  one 
of  the  most  striking  symptoms  is  the  lateral  deviation 
of  the  head  and  the  lateral  curvature  of  the  entire 
body. 

13.  Disturbances  in  Weight  Estimation. — A  symp- 
tom due  to  disturbance  of  the  sensory  impulses  was 
first  described  by  Lotmar  in  the  Monatsschr.  f.  Psy- 
chologie  ii.  Neurologie,  1908,  and  later  confirmed  by 
O.  ]Maas  and  others.  This  is  the  underestimation  of 
weights  by  the  hand  on  the  side  of  the  cerebellar 
lesion.  A  number  of  metal  discs  are  prepared  which 
are  the  same  in  size  but  differ  in  weight.  A  disc  is 
put  into  each  hand  and  the  patient  asked  to  judge 
whether  they  are  equal  or  not.  With  a  cerebellar 
abscess  on  the  right  side,  a  heavier  weight  in  the 
right  hand  will  seem  equal  to  a  lighter  weight  in  the 
left  hand.  This  symptom  must  be  judged  very  care- 
fully, for  in  right-handed  individuals  the  left  hand 
normally  overestimates  weight. 

The  symptoms  which  are  due  to  destruction  of  the 
fiber-tracts  between  the  vestibular  nuclei  and  the  cen- 
tral nuclei  of  the  cerebellum  are  nystagmus,  enduring 
nystagmus,  vertigo  and  vomiting. 

The  nystagmus  due  to  cerebellar  disease  cannot  be 
distinguished  from  that  due  to  disease  of  the  vestibu- 


132  CEREBELLAR  ABSCESS 

lar  apparatus.  It  varies  in  its  direction.  Nystag- 
mus was  noted  in  46  out  of  tlie  86  cases.  It  was 
directed  to  the  diseased  side  15  times,  to  the  sound 
side  7  times,  to  both  sides  22  times,  and  in  2  cases  the 
direction  was  not  mentioned. 

Of  40  cases  of  cerebellar  abscess  reported  by  Neu- 
mann, the  nystagmus  was  directed  toward  the  diseased 
side  17  times,  in  14  cases  the  direction  was  not  stated, 
and  in  9  cases  there  was  no  nystagmus. 

Although  the  appearance  of  cerebellar  nystagmus 
does  not  differ  from  that  of  labyrinthine  n^^stagmus, 
yet  its  behavior  does.  Labyrinthine  nystagmus,  M'hen 
due  to  a  diffuse  labyrinthitis,  gi'adually  diminishes  in 
intensity,  and  ceases  in  a  few  weeks.  The  direction 
of  such  a  nystagmus  is  always  away  from  the  diseased 
ear.  Cerebellar  nystagmus  remains  the  same  or  be- 
comes more  marked.  A  nystagmus  toward  an  ear  of 
which  the  labyrinthine  functions  are  destroyed,  cannot 
be  labyrinthine  in  origin.  It  must  be  retrolaby- 
rinthine,  probably  cerebellar.  In  some  cases,  there  is 
a  dead  labyrinth  with  nystagmus  toward  the  sound 
side.  During  the  course  of  the  disease,  the  nystagmus 
suddenly  changes  to  the  diseased  side.  This  usually 
indicates  a  cerebellar  abscess.  Sometimes  with  cere- 
bellar abscess  there  is  a  nystagmus  in  both  directions, 
rotatory  to  one  side  and  horizontal  to  the  other. 

The  nystagmus  of  a  circumscribed  labyrinthitis  is 
difficult  to  differentiate  from  that  of  a  cerebellar  ab- 


SYMPTOMS  133 

scess.  In  the  latter  case,  we  often  have  other  symp- 
toms of  intracranial  disease  to  guide  us.  Neumann 
recommends  doing  a  labyrinthectomy  in  cases  of 
doubt.  If  there  was  a  circumscribed  labyrinthitis,  the 
nystagmus  will  shift  toward  the  sound  side.  If  the 
nystagmus  remains  directed  to  the  diseased  side,  we 
are  dealing  with  a  cerebellar  abscess. 

Enduring  Nystagmus. — If  cold  water  be  allowed  to 
flow  into  an  ear,  and  the  flow  stopped  as  soon  as  nys- 
tagmus sets  in,  the  nystagmus  will  continue  from  one 
to  two  and  one-half  minutes  under  normal  conditions. 
In  cerebellar  disease,  the  caloric  nystagmus  which  is 
directed  toward  the  affected  hemisphere  will  continue 
for  five  to  ten  minutes,  or  even  longer,  and  is  more 
intense  than  normal.  This  is  called  by  Neumann 
"enduring  nystagmus,"  and  is  due  to  loss  of  the  inhib- 
itory control  which  the  cerebellum  exercises  over  the 
vestibular  centers. 

Vertigo  was  present  in  56  out  of  the  86  cases. 
There  is  nothing  characteristic  about  cerebellar  ver- 
tigo. Its  intensity  is  not  influenced  by  looking  in  dif- 
ferent directions,  as  vestibular  vertigo  is. 

Vomiting  occurred  in  48  of  the  cases.  It  may  occur 
with  or  without  nausea.  Vomiting,  accompanied  by 
nausea,  is  due  to  involvement  of  the  vestibulo-cerebel- 
lar  tracts. 

Of  the  above-mentioned  symptoms,  there  may  be 
only  one  or  a  few  present,  or  there  may  be  none  at  all. 


134  CEREBELLAR  ABSCESS 

The  cerebellar  abscess  may  be  found  only  at  autopsy. 
Okada  found  that  in  ten  per  cent  of  cases  of  cerebel- 
lar abscess,  death  occurred  before  any  symptoms  of 
intracranial  involvement  appeared. 

In  fourteen  per  cent  of  the  cases,  the  symptoms  of 
cerebellar  abscess  were  obscured  by  other  otitic  com- 
plications. 

In  forty-two  per  cent,  the  diagnosis  was  rendered 
very  difficult  on  account  of  the  presence  of  other 
intracranial  complications,  such  as  sinus-phlebitis, 
pachy-  or  leptomeningitis,  or  temporo-sphenoidal  lobe 
abscess. 

Not  all  cases  of  cerebellar  abscess  which  are  re- 
ported as  latent,  really  are  latent,  because  the  cere- 
bellar tests  are  not  always  made. 

Latent  cases  are  of  two  kinds: 

1.  Where  there  never  were  symptoms.  This  might 
be  due  to  separation  of  the  nervous  elements  without 
their  destruction.  This  is  more  probable  in  cases  of 
tumor  or  hemorrhage  than  with  abscess.  It  may  be 
due  to  involvement  of  a  silent  area  of  the  cerebel- 
lum. 

2.  Where  there  are  symptoms  at  the  beginning, 
which  later  disappear.  This  is  due  to  compensation. 
Cerebellar  symptoms  may  be  made  more  marked  and 
enduring  by  the  association  of  lesions  in  compensatory 
organs  (cerebrum,  labyrinth  or  sensory  paths) .  For 
instance,  in  disease  of  the  cerebello-pontine  angle,  the 


SYMPTOMS  135 

eighth  nerve  is  involved  along  with  the  cerehellum. 
This  causes  very  severe  symptoms. 

The  course  of  cerebellar  abscess  is  usually  divided 
into  four  stages,  the  initial  stage,  the  latent  stage,  the 
manifest  stage  and  the  terminal  stage. 

The  initial  stage  lasts  a  day  or  two  and  is  marked 
by  chills  or  chilly  feelings,  and  malaise.  It  is  usually 
not  noticed,  and  is  often  masked  by  the  symptoms  of 
the  ear  disease  which  is  the  etiological  factor. 

The  latent  stage  may  last  anywhere  from  a  few 
days  to  man^^  months  or  even  years.  It  is  not  really 
latent,  but  the  symptoms  are  usually  so  slight  that 
they  are  overlooked.  There  may  be  occasional  head- 
ache during  this  period,  with  vertigo  and  loss  of  appe- 
tite. 

During  the  manifest  stage,  any  of  the  symptoms 
above  described  may  appear.  Sometimes,  however, 
the  manifest  stage  may  be  entirely  wanting,  the  diag- 
nosis being  made  at  operation  or  autopsy.  The  mani- 
fest stage  may  last  several  weeks. 

The  terminal  stage  is  the  period  after  the  abscess 
has  ruptured  either  into  the  fourth  ventricle  or  onto 
the  surface  of  the  cerebellum,  and  its  symptoms  are 
those  of  the  resultant  meningitis. 

In  uncomplicated  cases,  death  may  be  due  to 

1.  Increasing  intracranial  pressure  with  edema  of 
the  brain. 

2.  Encephalitis. 


136  CEREBELLAR  ABSCESS 

3.  Toxic  coma. 

4.  Rupture  into  the  subarachnoid  space. 

5.  Rupture  into  tlie   fourth  ventricle. 

Differential  Diagnosis 

Cerebellar  abscess  must  be  differentiated  from  tem- 
poro-sphenoidal  lobe  abscess,  tumor  of  the  cerebellum 
or  of  the  eighth  nerve,  labyrinthitis,  meningitis,  epi- 
dural abscess,  sinus  thrombosis  and  hysteria. 

From  temporo-sphenoidal  lobe  abscess,  it  is  differ- 
entiated by  the  localizing  signs.  In  temporo-sphenoi- 
dal lobe  abscess,  there  may  be  aphasia  or  hemianopsia. 
There  may  be  hemianesthesia  and  hemiparesis  of  the 
opposite  side.  When  a  hemiparesis  is  present  in  cere- 
bellar abscess  it  is  on  the  side  of  the  lesion. 

The  disturbances  of  speech  which  may  be  present 
in  cerebellar  abscess  are  disturbances  in  articulation, 
in  contradistinction  to  the  aphasia  which  may  be  pres- 
ent in  temporo-sphenoidal  lobe  abscess. 

There  may  be  abnormalities  of  the  ocular  muscles 
in  both  conditions.  Nystagmus  is  very  common  in 
cerebellar  abscess,  but  very  rare  in  temporo-sphenoi- 
dal lobe  abscess.  In  cerebellar  abscess  there  may  be  a 
spontaneous  deviation  of  one  or  more  extremities,  a 
loss  of  the  reaction  movements  of  the  extremities,  or 
a  loss  of  the  reaction  movements  of  the  trunk. 

The  location  of  the  headaclie  is  not  characteristic. 


SYMPTOMS  137 

There  may  be  local  sensitiveness  to  percussion  over 
the  site  of  the  abscess.  Rigidit}^  of  the  neck  is  not 
uncommon  with  cerebellar  abscess. 

If  the  abscess  follows  labyrinthine  disease  or  sinus 
thrombosis,  it  is  more  apt  to  be  in  the  cerebellum  than 
in  the  temporo-sphenoidal  lobe. 

Cerebellar  abscess  is  differentiated  from  tumor  of 
the  cerebellum  by  the  fact  that,  in  the  former  condi- 
tion, there  is  a  middle-ear  suppuration.  In  abscess, 
there  may  be  some  fever,  although  it  is  never  very 
high.  In  tumor,  there  is  a  gradual  and  steady 
increase  in  the  severity  of  the  symptoms  which  may 
extend  over  a  considerable  period  of  time.  In  abscess, 
there  is  usually  a  period  of  latency,  and  then  a  rapid 
development  of  the  symptoms,  which  may  remain  con- 
stant vmtil  shortly  before  death,  at  which  time  symp- 
toms of  diffuse  meningitis  supervene.  In  tumor  of  the 
cerebellum  the  fundus  changes  are,  as  a  rule,  much 
more  marked  than  in  abscess. 

In  abscess  the  cerebro-spinal  fluid  may  show  an  in- 
crease in  the  polynuclear  white  cells,  and  bacteria  may 
be  present.  In  tumor,  the  fluid  is  more  likely  to  be 
normal.  In  the  latter  the  lymphocytes  may  be 
increased.  With  abscess  the  blood  may  show  increase 
in  the  leucocytes. 

In  tumor  of  the  eighth  nerve,  the  symptoms  are 
similar  to  those  of  cerebellar  tumor,  but  deafness  is 
usually  one  of  the  first  symptoms  to  appear,  and 


138  CEREBELLAR  ABSCESS 

symptoms  of  destruction  of  the  eighth  and  seventh 
nerves  are  very  prominent. 

Cerebellar  abscess  is  differentiated  from  labyrinthi- 
tis by  the  fact  that  there  is  no  headache  in  the  latter, 
but  usually  a  marked  headache  in  the  former.  The 
character  of  the  nystagmus  is  the  same  in  both  condi- 
tions, but  its  behavior  is  diflPerent.  In  cerebellar  ab- 
scess, the  nystagmus  may  be  directed  toward  the  af- 
fected side,  toward  the  sound  side,  or  in  both  direc- 
tions. It  may  be  rotatory  in  one  direction  and  hori- 
zontal in  the  opposite  direction.  In  manifest  diffuse 
suppurative  labyrinthitis,  the  nystagmus  is  always 
directed  away  from  the  diseased  ear.  In  circum- 
scribed labyrinthitis  it  is  usually  directed  toward  the 
diseased  ear. 

If  the  labyrinthine  tests  show  the  presence  of  a  dif- 
fuse labyrinthitis,  i.  e.,  if  there  is  complete  deafness 
and  a  negative  caloric  reaction  in  the  ear,  and  the  nys- 
tagmus is  directed  toward  the  diseased  ear,  the  nystag- 
mus cannot  be  due  to  the  labyrinthine  disease.  Pro- 
vided the  opposite  ear  is  normal,  it  must  be  retrolaby- 
rinthine  in  origin,  and  is  probably  cerebellar. 

In  diffuse  labyrinthitis,  the  intensity  of  the  nystag- 
mus steadily  diminishes  and  subsides  entirely  in  two 
or  three  weeks.  In  cerebellar  abscess  it  may  remain 
imchanged  for  a  long  time  or  even  become  more 
marked. 

Neither  the   direction   of   the   nystagmus   nor   its 


SYMPTOMS  139 

duration  differentiates  between  cerebellar  abscess  and 
circumscribed  labyrinthitis.  In  both  conditions,  it 
may  be  directed  toward  the  diseased  side,  and  may 
last  a  long  time.  Where  it  is  not  possible  to  differen- 
tiate between  the  two  conditions,  Neumann  advises 
doing  a  labyrinthectomy.  If  there  was  a  circum- 
scribed labyrinthitis  present,  the  nystagmus  will 
change  to  the  sound  side.  If,  however,  there  is  a  cere- 
bellar abscess  present,  the  nj^stagmus  will  remain  di- 
rected toward  the  diseased  side. 

Changes  may  be  present  in  the  cerebro-spinal  fluid. 
The  fluid  is  usually  normal  in  uncomplicated  labyrin- 
thine disease. 

Spontaneous  deviation  and  loss  of  reaction  move- 
ments may  be  present  in  cerebellar  abscess.  In  cere- 
bellar abscess,  the  spontaneous  deviation  of  the  ex- 
tremities and  the  tendency  to  fall  bear  no  definite 
relationship  to  the  spontaneous  nystagmus,  nor  does 
the  direction  of  the  falling  change  with  alterations  in 
the  position  of  the  head.  With  labyrinthine  disease, 
the  spontaneous  deviations  of  the  extremities  and  the 
falling  are  always  in  the  direction  of  the  slow  compo- 
nent of  the  spontaneous  nystagmus,  and  the  spon- 
taneous falling  and  deviations  change  with  alterations 
in  the  position  of  the  head.  The  reaction  movements 
are  present  in  labyrinthine  disease. 

Cerebellar  abscess  is  differentiated  from  meningitis 
by  the  following  facts:    The  duration  of  a  cerebellar 


140  CEREBELLAR  ABSCESS 

abscess  is  usually  weeks  or  months,  that  of  a  meningi- 
tis is  only  days.  The  temperature  in  cerebellar  ab- 
scess is  usually  low.  It  may  be  normal  or  even  sub- 
normal. In  meningitis  it  is  usually  high.  The  pulse 
is  usually  slow  in  abscess.  In  meningitis  it  is  rapid. 
There  is  not  usually  much  disturbance  of  the  sen- 
sorium  in  abscess.  In  meningitis  there  is  marked  dis- 
turbance of  the  sensorium,  often  complete  coma. 
Optic  nerve  changes  are  more  common  in  abscess  than 
in  meningitis.  Focal  signs  are  common  in  abscess. 
They  are  rare  in  meningitis.  Kernig's  sign,  Babin- 
ski's  sign,  ankle-clonus,  increase  of  the  knee-jerks, 
etc.,  are  not  often  seen  in  abscess.  The  spinal  fluid 
in  an  abscess  may  be  normal,  or  may  contain  an  in- 
crease in  the  white  cells.  In  meningitis  it  contains  an 
increased  number  of  white  cells  and  bacteria.  Cere- 
bellar abscess  is  complicated  by  meningitis  at  the  end 
and  the  symptoms  of  the  latter  condition  then  obscure 
those  of  the  former. 

Tuberculous  meningitis  resembles  abscess  more 
than  diffuse  purulent  meningitis  does,  because  in  tu- 
berculous meningitis  the  temperature  is  apt  to  be 
lower,  and  there  is  a  tendency  to  localization.  In 
serous  meningitis,  the  signs  of  increased  intracranial 
pressure  stand  in  the  foreground.  There  are  usually 
no  focal  signs.  Lumbar  puncture  discloses  a  nor- 
mally constituted  fluid  under  increased  pressure. 

Epidural  abscess  is  rarely  confounded  with  cere- 


SYMPTOMS  141 

bellar  abscess.  The  former  is  usually  found  at  opera- 
tion, without  being  suspected  beforehand. 

It  sometimes  causes  marked  headache,  but  its  symp- 
toms are  usually  masked  by  the  accompanying  mas- 
toid disease.  Epidural  abscess  is  often  present  with 
cerebellar  abscess. 

Hysteria  may  be  mistaken  for  cerebellar  abscess. 
Hysterical  patients  may  have  headache  and  vertigo 
and  even  hemiparesis  and  hemianesthesia;  but  they 
have  no  spontaneous  deviations  or  loss  of  reaction 
movements.  They  have  no  nystagmus,  ej^e-ground 
changes,  fever,  slow  pulse  or  emaciation. 

The  diagnosis  of  cerebellar  abscess  is  sometimes 
made  from  the  findings  at  the  mastoid  operation.  A 
fistula  may  be  seen  in  the  dura  leading  to  the  cere- 
bellar abscess.  There  may  be  discoloration  of  the 
dura,  or  perhaps  lack  of  pulsation  of  the  cerebel- 
limi. 

When  cerebellar  abscess  is  suspected,  it  is  some- 
times advisable  to  do  a  radical  mastoid  operation,  and 
expose  the  dura  of  the  posterior  cranial  fossa.  If 
there  are  no  local  signs  in  the  dura  to  warrant  one 
in  exploring  the  cerebellum,  it  is  advisable  to  await 
developments.  If  there  is  no  cerebellar  abscess  pres- 
ent, the  symptoms  may  subside  after  the  operative 
interlocution.  If  the  sjTnptoms  persist,  the  cerebel- 
lum can  be  explored  several  days  later.  It  is  safer 
to  explore  the  cerebellum  at  this  time,  as  adhesions 


142  CEREBELLAR  ABSCESS 

have  formed  between  the  dura  and  pia,  and  there  is 
less  likehhood  of  infecting  the  meninges  by  the  ex- 
ploratory punctures  or  incisions.  However,  where 
there  are  definite  localizing  signs  of  cerebellar  abscess, 
it  is  not  necessary  to  wait. 


CHAPTER  V 

PROGNOSIS    AND    TREATMENT    OF    CEREBELLAR    ABSCESS 


CHAPTER  V 

PROGNOSIS  AND  TREATMENT  OF  CEREBELLAR  ABSCESS 

CEREBELLAR  abscess,  if  untreated,  is  al- 
most surely  fatal.  A  few  cases  of  sponta- 
neous cure  have  been  reported  in  the  litera- 
ture, but  such  an  outcome  must  be  so  rare  that  it 
should  be  given  no  weight  whatever  in  the  considera- 
tion of  the  indications  for  treatment.  It  is  possible 
that  a  very  small  abscess  may  undergo  resorption 
and  thus  get  well.  Those  cases  of  cerebellar  ab- 
scess which  rupture  into  the  mastoid,  and  from  which 
pus  finds  exit  through  a  perforation  in  the  drum-mem- 
brane or  through  a  fistula  in  the  skin  over  the  outer 
surface  of  the  mastoid,  do  not  get  well.  The  fistula  is 
too  narrow  and  tortuous  to  permit  adequate  drainage 
of  the  abscess.  From  time  to  time  the  fistula  may 
become  occluded  and  there  is  a  lighting  up  of  the 
brain  symptoms,  and  then  if  there  is  a  re-establish- 
ment of  drainage,  the  symptoms  may  subside. 

The  only  treatment  for  cerebellar  abscess  is  opera- 
tion. AVe  can  safely  say  that  practically  all  cases  of 
cerebellar  abscess  which  are  not  operated  upon  die. 

The  percentage  of  recoveries  from  cerebellar  abscess 
following  operation  varies  in  the  hands  of  different 

145 


146  CEREBELLAR  ABSCESS 

operators,  and  after  different  operative  procedures. 
Macewen,  as  far  back  as  1893,  reported  a  series  of 
19  cases  of  brain  abscess,  of  which  he  cured  18  by 
operation.  Of  these,  13  were  otogenous,  9  being  sit- 
uated in  the  temporo-sphenoidal  lobe  and  4  in  the 
cerebelhim.  Xo  other  surgeon  has  been  able  to  equal 
this  record. 

Koerner  reported  55  cases  of  operations  for 
cerebellar  abscess  in  1901,  of  which  52.8  per  cent  were 
cured. 

Heimann  collected  519  operations  for  brain  abscess 
in  1908.  Of  these  323  were  in  the  cerebrum  and  196 
in  the  cerebellum.  One  hundred  and  ninety-three 
(37.08  per  cent)  got  well.  Of  the  healed  cases,  144 
were  in  the  temporo-sphenoidal  lobe,  40  in  the  cere- 
bellum, and  3  in  the  temporo-sphenoidal  lobe  and 
cerebellum. 

Oppenheim  and  Cassirer  collected  76  cases  of  oper- 
ations for  cerebellar  abscess  in  1909.  Of  these  35 
(44.9  per  cent)  were  cured. 

Dench  collected  102  operations  for  cerebellar  ab- 
scess, of  which  33  recovered.  Koch  reported  25  cases 
of  operations  for  cerebellar  abscess  of  which  16  were 
cured. 

Neumann  collected  101  cases  of  cerebellar  abscess 
operated  upon,  of  which  40  recovered. 

The  results  of  operation  for  cerebellar  abscess  are 
not  as  favorable  as  those  for  temporo-sphenoidal  lobe 


PROGNOSIS  AXD  TREATMENT     147 

abscess.  This  is  due  to  the  fact  that  it  is  easier  to 
drain  an  abscess  in  the  temporo-sphenoidal  lobe  than 
in  the  cerebelhim.  Furthermore,  abscesses  in  the  cere- 
bellum are  so  close  to  the  respiratory  center  in  the 
medulla  that  manipulations  in  this  region  can  easily 
cause  respiratory  paralysis. 

In  most  of  the  statistics,  the  percentage  of  recov- 
eries is  probably  given  too  high,  since  favorable  cases 
are  more  apt  to  be  reported  than  unfavorable  ones. 
Furthermore,  many  of  the  cases  are  reported  too 
early.  A  case  should  not  be  reported  as  cured  unless 
it  has  remained  well  for  at  least  six  months  after  the 
operation;  for  it  is  not  an  uncommon  experience  for 
a  patient  to  be  apparently  well  for  several  months 
after  an  operation  for  cerebellar  abscess,  and  then  sud- 
denly develop  meningitic  symptoms  and  die. 

A  patient  with  cerebellar  abscess  is  never  too  sick 
to  be  operated  on.  He  may  be  moribund,  and  yet 
recover  after  the  operation.  Symptoms  of  meningi- 
tis are  no  contraindication  to  operation,  as  sometimes 
the  symptoms  of  a  cerebellar  abscess  are  very  similar 
to  those  of  meningitis. 

The  causes  of  death  from  cerebellar  abscess,  with 
or  without  operation,  according  to  von  Bergmann,  are 
as  follows : 

1.  Rupture  of  the  abscess  into  the  fourth  ventricle. 

2.  Rupture  onto  the  surface  of  the  cerebellum  with 
a  resultant  leptomeningitis. 


148  CEREBELLAR  ABSCESS 

3.  The  abscess  cannot  be  found  at  operation. 

4.  There  is  a  second  abscess. 

5.  The  abscess  has  more  than  one  chamber. 

6.  The  encephahtis  progresses  in  spite  of  evacua- 
tion of  the  abscess. 

7.  Sinus  thrombosis  with  pyemia. 

8.  Pneumonia. 

9.  Shock. 

10.  Respiratory  failure. 

By  far  the  most  common  cause  of  death  is  purulent 
leptomeningitis. 

The  prognosis  is  most  favorable  in  those  cases  in 
which  the  abscess  is  near  the  surface  of  the  cerebellum, 
especially  when  there  is  a  fistula  through  the  dura, 
and  when  there  is  a  firm  capsule  about  the  abscess. 
The  unfavorable  cases  are  those  in  which  the  abscess 
is  situated  far  from  the  surface  and  has  no  capsule. 

The  prophylactic  treatment  consists  in  the  treat- 
ment of  the  causes  of  cerebellar  abscess,  namely,  laby- 
rinthitis, sinus  thrombosis  and  epidural  abscess.  Sup- 
purative labyrinthitis  is  treated  by  means  of  a  radical 
mastoid  operation  and  labyrinthectomy.  Sinus* throm- 
bosis is  treated  by  opening  the  sinus,  removing  the 
thrombus,  and  tying  off  or  resecting  the  internal  jug- 
ular vein.  Epidural  abscess  is  treated  by  removing 
the  inner  table  over  the  abscess. 

Operations  on  the  brain  are  best  done  under  chloro- 
form anesthesia.     Ether  causes  a  congestion  of  the 


PROGNOSIS  AND  TREATMENT     149 

brain  and  increases  the  tendency  to  edema  of  the  brain 
tissue,  whereas  chloroform  diminishes  the  congestion 
of  the  brain.  This  factor  is  more  important  in  opera- 
tions on  the  cerebellum  than  in  those  on  the  cerebrum, 
on  account  of  the  danger  of  respiratory  paralysis  from 
pressure  of  the  swollen  cerebellum  upon  the  medulla. 
When  the  operation  is  done  in  two  stages,  the  dura 
being  exposed  at  the  first  operation,  the  second  stage 
requires  very  little  anesthesia,  as  the  brain  tissue  pos- 
sesses little  sensation. 

Although  the  methods  of  approach  may  differ  in 
various  cases,  the  treatment  of  cerebellar  abscess  must 
be  based  upon  two  principles.  The  first  is  the  estab- 
lislmient  and  maintenance  of  efficient  drainage;  the 
second  is  adequate  decompression  so  that  the  edema 
of  the  brain  which  threatens  the  vital  centers  may  be 
relieved. 

In  the  first  place  it  must  be  remembered  that  the 
vast  majority  of  cerebellar  abscesses  are  situated  in 
the  anterior  portion  of  this  organ.  This  is  to  be  ex- 
pected when  one  recalls  that  infection  of  the  cere- 
bellum is  usually  secondary  to  a  suppurative  labyrin- 
thitis, an  epidural  abscess  in  the  posterior  fossa  or  a 
thrombo-phlebitis  of  the  sigmoid  portion  of  the  lateral 
sinus. 

The  operative  treatment  of  cerebellar  abscess  varies 
according  to  the  findings.  (Figs.  21-23.)  The 
method   of  approach  will  materially  vary  with   the 


1.50  CEREBELLAR  ABSCESS 

pathway  of  the  brain  infection.  When  a  cerebellar 
abscess  is  suspected,  a  simple  or  a  radical  mastoid 
operation  is  done.  In  cases  of  acute  middle-ear  sup- 
puration, a  simple  mastoid  operation  is  done,  and  in 
chronic  middle-ear  suppuration,  a  radical  mastoid 
operation.  The  inner  table  is  removed,  exposing  the 
dura  of  the  posterior  fossa. 

In  all  cases,  irrespective  of  the  pathway  of  infec- 
tion, a  wide  decompression  of  the  posterior  fossa 
should  be  done,  continuing  the  removal  of  bone  well 
down  underneath  the  cerebellum  toward  the  foramen 
magnum. 

If  the  dura  is  found  to  be  normal,  and  the  symp- 
toms of  cerebellar  abscess  are  only  suggested,  it  is 
w^ise  to  wait,  for  sometimes  the  disease  in  the  temporal 
bone  may  give  symptoms  similar  to  those  of  intra- 
cranial disease,  and  these  symptoms  will  subside  after 
the  mastoid  operation. 

The  exposure  of  the  dura  will  produce  adhesions 
between  the  dura  and  the  surface  of  the  cerebellum, 
so  that  if  the  symptoms  do  not  subside  after  the  mas- 
toid operation  and  it  becomes  necessary  to  incise  the 
dura,  infection  of  the  meninges  is  less  likely  to  occur. 

Labyrinthine  disease  is  especially  liable  to  simulate 
cerebellar  abscess.  If  the  functional  tests  show  a  dead 
labyrinth,  i.  e.,  if  there  is  complete  deafness  in  the 
affected  ear  and  a  negative  caloric  reaction,  and  the 
nystagmus  is  directed  toward  the  sound  side,  we  may 


Fig.  21. — Operation  for  Cerebellar  Abscess. 
A  radical  mastoid  operation  has  been  done.     Sinus  is  being  un- 
covered bv  chisel. 


151 


Fig.  22. — Operation   for  Cerebellar  Absc  kss. 

Sinus   and   cerebellar   dura   exposed.      Incision    through   dura    in 

front  of  and  behind  sinus. 


153 


Fig.  23. — Operation  for  Cerebellar  Abscess. 

Labyrinthectomy.      Internal    auditory    canal    exposed.      Incision 

throush  cerebellar  dura  in  front  of  sinus. 


155 


PROGNOSIS  AND  TREATMENT    157 

have  either  a  diffuse  suppurative  labyrinthitis  alone, 
or  a  diffuse  suppurative  labyrinthitis  complicated  by 
a  cerebellar  abscess.  A  labyrinthectomy  is  done,  and 
the  dura  of  the  posterior  fossa  exposed.  If  the  dura 
looks  normal,  it  is  not  incised  unless  there  be  positive 
signs  of  cerebellar  involvement.  The  patient  is  care- 
fully watched,  and  if  the  symptoms  were  due  to  the 
labyrinthitis  alone,  they  will  improve  in  a  few  days. 
The  symptoms  of  an  acute  diffuse  suppurative  laby- 
rinthitis reach  their  maximum  intensity  Avithin  twenty- 
four  hours,  and  then  show  a  gradual  improvement 
from  day  to  day.  If  the  symptoms  do  not  clear  up 
in  a  short  while,  the  cerebellum  should  be  explored 
for  an  abscess. 

If  the  functional  tests  show  a  dead  labyrinth,  and 
the  nystagmus  is  directed  toward  the  diseased  side, 
there  is  probably  a  cerebellar  abscess  complicating  a 
diffuse  suppurative  labyrinthitis,  for  a  dead  laby- 
rinth cannot  cause  a  nystagmus  toward  its  own  side. 
In  such  a  case,  the  cerebellum  is  explored  immedi- 
ately. 

If  the  functional  tests  show  a  normal  labyrinth,  a 
radical  mastoid  operation  is  done  and  the  posterior 
fossa  exposed.  If  an  epidural  abscess  is  found  and 
a  fistula  leading  into  a  cerebellar  abscess,  the  dura  is 
first  cleaned  thoroughly  with  saline  followed  by  alco- 
hol. Michaelsen  advises  mopping  the  dura  with  tinc- 
ture of  iodin.    After  the  dura  is  thoroughly  cleaned. 


158  CEREBELLAR  ABSCESS 

a  knife  is  introduced  into  the  fistula  and  the  abscess 
slit  open  for  three  or  four  centimeters. 

If  the  dura  of  the  posterior  fossa  is  normal,  it  is 
sometimes  advisable  to  expose  the  dura  of  the  middle 
fossa,  for  temporo-sphenoidal  lobe  abscess  occasion- 
ally gives  rise  to  symptoms  very  similar  to  those  of 
cerebellar  abscess.  If  nothing  abnormal  is  found 
here,  the  cerebellimi  is  explored.  The  cerebellum 
should  never  be  explored  through  an  intact  dura,  for 
the  following  reasons: 

1.  The  exploring  needle  or  knife  may  wound  a 
meningeal  vessel  of  some  size  and  cause  a  subdural 
hemorrhage,  which,  finding  no  escape,  may  cause  dan- 
gerous pressure  upon  the  cerebellum. 

2.  If  the  abscess  is  found,  some  pus  may  follow 
the  needle,  as  it  is  withdrawn,  and,  flowing  into  the 
subdural  space,  give  rise  to  a  diffuse  meningitis. 

3.  If  the  needle  is  plunged  through  a  pathologically 
thickened  and  inflamed  dura,  it  may  carry  some  of 
the  bacteria  which  are  lodged  in  the  deeper  layers  of 
the  dura  into  the  brain  tissue. 

It  is  best  to  incise  the  dura  before  exploring  the 
cerebellum.  The  point  at  which  the  cerebellum  is 
first  explored  is  Trautmann's  triangle.  This  is  a  tri- 
angle whose  upper  margin  is  formed  bj^  the  superior 
petrosal  sinus,  its  posterior  margin  by  the  anterior 
margin  of  the  lateral  sinus,  and  its  anterior  margin 
by  the  posterior  semicircular  canal.    The  apex  of  this 


PROGNOSIS  AND  TREATMENT     159 

triangle  is  directed  downward  and  is  in  the  region  of 
the  saccus  endolymphaticus,  and  the  base  of  the  trian- 
gle is  directed  upward.  A  hollow  needle  or  a  knife  or 
a  pair  of  forceps  may  be  used  to  explore  the  cerebel- 
lum. The  disadvantages  of  a  hollow  needle  are  that 
the  contents  of  the  abscess  may  be  so  thick  that  they 
cannot  be  drawn  through  the  canula,  or  the  lumen 
may  become  obstructed  by  a  piece  of  brain  tissue  be- 
fore it  reaches  the  abscess.  The  disadvantages  of  a 
knife  are  that  a  greater  extent  of  brain  tissue  is 
injured  than  with  a  needle,  and  there  is  greater  likeli- 
hood of  injuring  a  large  vessel.  With  blunt  forceps, 
there  is  less  danger  of  bleeding.  On  the  whole,  the 
knife  has  seemed  the  most  reliable  instrument  to  us. 
After  the  abscess  is  found,  the  incision  may  be  dilated 
by  means  of  forceps.  If  a  needle  is  used,  leave  the 
needle  in  situ  when  the  abscess  is  found,  and  run  the 
knife  along  this  as  a  guide. 

Before  the  drainage  tube  is  introduced  into  the 
abscess  a  free  dural  incision  is  made  in  order  to  attain 
sufficient  decompression.  A  linear  or  semicircular 
incision  is  preferable  to  a  cross  incision,  as  the  latter 
is  conducive  to  brain  hernia. 

The  needle  or  knife  is  passed  through  Trautmann's 
triangle  into  the  cerebellum  in  various  directions,  until 
the  abscess  is  discovered.  It  should  not  be  allowed 
to  pass  in  further  than  two  and  one-half  to  three  cm., 
in  order  to  avoid  entering  the  fourth  ventricle.     The 


160  CEREBELLAR  ABSCESS 

blade  of  the  knife  or  the  needle  may  be  marked  off  in 
centimeters.  If  the  abscess  is  not  found  in  Traut- 
mann's  triangle,  the  cerebellum  is  explored  behind  the 
lateral  sinus.  The  cerebellar  hemisphere  is  widely  ex- 
posed here  by  the  removal  of  a  portion  of  the  occipital 
bone,  and  the  dura  is  incised.  Krause  advises  making 
a  U-shaped  flap  in  the  dura,  and  packing  off  the  sub- 
dural space  by  means  of  a  strip  of  gauze  at  the  edges 
of  the  dural  incision.  In  this  way  every  drop  of  pus 
which  passes  out  of  the  cerebellar  incision  can  be 
mopped  up,  and  there  is  very  little  danger  of  causing 
a  diffuse  purulent  meningitis. 

The  area  through  which  the  searcher  is  being  passed 
should  be  protected  by  pledgets  of  cotton  wet  with 
warm  saline.  If  a  canula  be  used,  when  the  abscess 
is  found  and  pus  makes  its  appearance  at  the  proximal 
end  of  the  canula,  it  may  be  sucked  away  by  means  of 
a  suction  apparatus.  It  must  be  understood  that  suc- 
tion should  not  be  applied  through  the  canula.  JNIerely 
the  drops  of  pus  as  they  flow  out  of  the  mouth  of 
the  canula  should  be  sucked  away.  In  this  way  the 
field  does  not  become  soiled.  Forcible  aspiration  of 
the  contents  of  the  abscess  is  not  devoid  of  danger. 

When  the  abscess  is  found  and  the  pus  evacuated, 
a  drainage  tube  is  inserted  into  the  cavity.  It  is  not 
advisable  to  wash  out  the  abscess  cavity  nor  to  intro- 
duce the  finger,  or  encephaloscope,  as  such  interven- 
tions increase  the  encephalitis.    It  seems  that  the  cere- 


PROGNOSIS  AND  TREATMENT     161 

bellum  will  bear  less  handling  than  the  cerebrum.  For 
drainage  material,  rubber  tubing  or  a  decalcified 
chicken-bone  tube  seems  to  be  the  best.  UiFenorde 
and  ]Michaelsen  use  a  glass  tube,  with  a  gauze  wick 
inside.  Cigarette  drains  or  gauze  packing  do  not 
seem  to  be  very  effective,  as  they  cause  a  retention  of 
secretions.  It  is  advisable  to  have  several  perforations 
at  the  sides  of  the  tube  in  case  the  end  of  the  tube 
becomes  blocked  by  pieces  of  necrotic  tissue.  The 
outer  end  of  the  tube  is  surrounded  by  iodoform  gauze, 
and  a  dressing  applied.  It  may  be  necessary  to  hold 
the  tube  in  place  by  means  of  a  safety-pin  passed 
through  it.  The  dressings  are  changed  every  day  or 
even  oftener,  depending  upon  the  amount  of  secre- 
tion. The  tube  is  gradually  shortened  as  the  ab- 
scess diminishes  in  size,  and  is  finally  left  out  alto- 
gether. 

Some  otologists  prefer  to  explore  the  cerebellum 
through  the  occipital  bone  instead  of  through  the 
mastoid.  In  this  way  they  avoid  carr^^ing  infection 
into  the  cerebellum  from  the  infected  mastoid  cavity. 
However,  this  advantage  is  overweighed  by  several 
disadvantages,  viz. : 

1.  Cerebellar  abscesses  are  usually  located  near  the 
median  portion  of  the  ventral  surface  of  the  cerebel- 
lum, and  are  reached  most  easily  through  the  mas- 
toid. 

2.  Exposure  of  the  cerebellar  dura  through  the 


162  CEREBELLAR  ABSCESS 

mastoid  often  gives  valuable  information  as  to  the 
presence  of  an  abscess. 

3.  The  mastoid  operation  removes  the  primary- 
cause  of  the  cerebellar  infection. 

The  operation  through  the  occiput  is  done  as  fol- 
lows (Fig.  24) :  An  inverted  U-shaped  incision  is 
made  through  the  skin  and  the  periosteum  over  the 
occiput.  The  anterior  limb  of  this  incision  extends 
along  the  posterior  margin  of  the  mastoid,  the  upper 
limb  along  the  external  occipital  crest  and  the  pos- 
terior limb  along  the  middle  line  of  the  skull  down  to 
the  root  of  the  neck.  The  periosteum  is  reflected 
from  the  bone.  A  trephine  opening  is  made  through 
the  middle  of  the  exposed  bone,  and  the  opening  en- 
larged by  means  of  a  rongeur  forceps  until  the  lateral 
sinus  is  seen  above,  the  sigmoid  sinus  laterally,  and 
the  occipital  sinus  mesially.  A  U-shaped  dural  flap 
is  now  made  parallel  to  the  edges  of  the  bone  wound, 
and  the  subdural  space  packed  off  by  means  of  a  strip 
of  iodoform  gauze  which  is  inserted  between  the  dura 
and  the  surface  of  the  cerebellum.  The  cerebellum  is 
then  explored  for  the  abscess  with  a  knife,  grooved 
director,  or  needle. 

In  some  cases,  when  the  abscess  is  opened  through 
an  incision  in  Trautmann's  triangle,  a  counter  open- 
ing may  be  made  behind  the  lateral  sinus,  and  through 
and  through  drainage  instituted.  When  the  lateral 
sinus  is  thrombosed,  it  is  opened,  and  an  incision  made 


Fig.  2i. — Operation  for  Cerebellar  Abscess. 
Cerebellum  uncovered   from  behind. 


163 


PROGNOSIS  AND  TREATMENT     165 

through  the  inner  wall  of  the  sinus.  In  this  way 
verj^  free  access  can  be  gotten  to  the  cerebellum. 

The  following  procedure  has  been  suggested  by  us,  ^ 
and  while  we  have  had  no  personal  experience  with 
it,  Bourguet,  in  a  single  case  of  cerebellar  abscess,  has 
carried  it  to  a  successful  issue.  The  procedure  entails 
the  sacrifice  of  the  lateral  sinus  and  while  this  must  be 
carefully  considered,  it  seems  to  us  that  in  a  compli- 
cation as  formidable  as  cerebellar  abscess,  the  advan- 
tages gained  by  such  a  sacrifice  make  it  well  worth 
while. 

The  cerebellar  dura  is  exposed  in  front  of  and  be- 
hind the  sinus.  A  small  incision  is  made  in  the  dura 
in  front  of  the  sigmoid  sinus  just  below  the  knee. 
Through  this  incision  an  aneurysm  needle  threaded 
with  chromic  gut  is  passed,  from  before  backward, 
around  the  sinus,  until  the  blunt  threaded  point  pre- 
sents underneath  the  dura  behind  the  sinus.  The  dura 
on  the  point  of  the  aneurysm  needle  is  then  incised 
and  the  needle  pushed  through. 

The  chromic  gut  is  then  tied.  A  similar  ligature  is 
placed  around  the  sinus  as  close  as  possible  to  its  hori- 
zontal portion.  The  outer  wall  of  the  sinus  between 
the  ligatures  is  opened  and  cut  away.  Such  an  ex- 
posure affords  an  ideal  approach  to  collections  of  pus 
within  the  cerebellum. 

^  Since  the  above  was  written  we  have  learned,  through  a  private 
communication  from  Dr.  Edward  B.  Dench,  that  Mr.  Ballance,  of 
London,   has   also   successfully   used   this   procedure. 


166  CEREBELLAR  ABSCESS 

Koerner  gives  the  following  statistics  of  139  cases 
of  brain  abscess  operated  upon  by  various  methods : 

Cure.     Death. 

1.  Abscess   opened   through    diseased 

temporal  bone 22  14 

2.  Abscess    opened    through  diseased 

temporal    bone    with    counter 

opening  through  outside 4  0 

8.  Abscess  opened  through  fistula  on 

outer  surface  of  skull 4  0 

4.  Abscess  opened  through  outer  wall 

of  skull 42  52 

5.  jNIethod  not  given 0  1 

The  after  treatment  of  cerebellar  abscess  consists  of 
absolute  rest  in  bed.  Everything  should  be  avoided 
which  causes  hyperemia  of  the  brain.  The  amount 
of  secretion,  the  temperature  and  the  pulse  are  the 
guides  for  the  frequency  of  the  dressings.  If  symp- 
toms indicate  retention  of  secretions,  the  dressings 
must  be  changed  and  the  drainage  tube  inspected  and 
cleaned  out.  It  may  be  necessary  to  search  for  a  sec- 
ond abscess  or  for  a  pocket  in  the  first  abscess. 

If  a  radical  mastoid  operation  was  done,  a  secon- 
dary plastic  should  be  made  only  after  the  abscess  is 
entirely  healed. 

The  commonest  complication  following  operation 
for  cerebellar  abscess  is  prolapse  of  the  brain.  This 
is  due  to  encephalitis,  to  the  fact  that  the  abscess  w^as 


PROGNOSIS  AND  TREATMENT     167 

not  found,  or  that  a  pocket  remains  which  was  not 
opened,  or  that  there  is  a  second  abscess. 

When  it  is  due  to  an  unopened  pocket  or  a  second 
abscess,  it  recedes  after  evacuation  of  the  pus.  If  no 
pus  is  found,  an  attempt  is  made  to  cause  it  to  recede 
by  means  of  a  firm  pressure  bandage.  This  is  success- 
ful in  most  cases,  although  in  extreme  cases  it  may 
take  several  weeks.  If  this  is  not  successful  it  may 
be  necessary  to  excise  the  prolapse.  As  the  prolapse 
consists  largely  of  edematous  tissue,  and  contains  very 
little  normal  brain  tissue,  this  intervention  is  not  as 
serious  a  one  as  may  appear.  The  prolapse  may  be 
made  to  recede  by  doing  a  lumbar  puncture.  After 
a  successful  operation  for  cerebellar  abscess,  the  im- 
provement is  immediate.  The  sensorium  improves. 
The  pulse  increases  rapidly.  The  paralytic  signs 
usually  clear  up.  Some  of  the  symptoms  may  remain 
permanently.  These  are  the  symptoms  which  are  due 
to  actual  destruction  of  tissue.  Cysts  and  cicatrices 
may  remain  after  operation  and  give  rise  to  attacks 
of  epilepsy. 


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Matthewson,  G.  H. — "Cerebellar  Abscess  of  Otitic  Origin; 
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Meyers,  I.  L. — "  Galvanometric  Studies  of  the  Cerebellar 
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MiCHAELSON,  M. — "Zur  Klinik  der  otitischen  Hirnabszesse. " 
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MiLLiGAN,  W. — "Two  Cases  of  Cerebellar  Abscess."  Pro- 
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Mills,  C.  K.,  and  Weisenburg,  T.  II. — "Cerebellar  Symp- 
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BIBLIOGRAPHY  177 

Morton,  J.  P. — "Lateral  Sinus  Thrombosis  and  Cerebellar 
Abscess. ' '  Dominion  Medical  Monthly,  1908,  Vol.  XXXI, 
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Neumann,  H. — "Cerebellar  Abscess."     1907. 

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Oppenheim,  H.,  and  Cassirer,  R. — "Der  Hirnabszess. " 
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Paterson,  D.  R. — "Treatment  of  Otitic  Cerebellar  Abscess; 
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INDEX 


INDEX 


Abscess,  cerebellar.    See  Cerebellar 
abscess, 
contents  of,  98. 
epidural,  8i?,  83,  140,  141,  157. 

Accessory  brachium  conjunctivum, 
36,'  41. 

Adhesions,  150. 

Adiadokokinesis,  102,  111. 

After-treatment   of  cerebellar   ab- 
scess, 166. 

Age  in  cerebellar  abscess,  77. 

Alae  lobi  centralis,  23. 

Anesthesia  in  cerebellar  operations, 
148,  149. 
corneal,  107. 

Ankle-clonus,  140. 

Anterior  crescentic  lobes,  23. 

Anterior  horn  cells,  30. 

Aqueduct  of  Sylvius,  19. 

Association    fibers    of    cerebellum, 
32. 

Asynergy,  102,  110. 

Atony,  70,  103,  113. 

Auditory  meatus,  internal,  19,  26. 

Babinski's  sign,  140. 
Ballance,  165. 
Barany,  60,  61,  114. 
Barany,  tonus  centers  of,  67. 
Basket  cells,  32. 
Bechterew's  nucleus,  2G,  56. 
vox  Bergmann,  147. 
BiNG,  60. 

Biventral  lobes,  23. 
Blood  changes,  105,  108. 

BOURGUET,    165. 

Brachium  conjunctivum,  36,  41. 

accessory,  36,  41. 
Bradycardia,  106. 
Brain,  prolapse  of,  166,  167. 

sensitiveness  of  tissue  of,  149. 

Capsule  of  cerebellar  abscess,  96. 
Cassirer,  146. 
Catalepsy,  103,  114. 
Centrifugal  fibers,  32. 
Centripetal  fibers,  32,  33. 


Cerebellar  abscess,  after-treatment 
of,  166. 

age  in,  77. 

bacteriology  of,  99. 

capsule  of,  96. 

deep,  88,  89. 

latency  of,  134. 

operation  for,  in  two  stages,  149 
method    of   approach   in,    149, 

150 
through  sinus  walls,  165 

recoveries   after,   146. 

sex  in,  77. 

situation  of,  88. 

spontaneous  cure  of,  145. 

stages  of,  135. 

superficial,  88,  89. 
Cerebellar  fissures,  21,  23. 
Cerebellar  lobes,  21,  23. 
Cerebellar  localization,  61. 
Cerebello-thalamic  bundle,  ventral, 

36. 
Cerebello-pontine  angle,  19. 
Cerebellum,    association    fibers    of, 
32. 

central  nuclei  of,  26,  30,  33,  36. 

cortex  of,  26. 

electric  stimulation  of,  59. 

exploration  of,  through  occiput, 
161,  162. 

inhibitory  control  of,  69. 

laminae  of,  26. 

motor  impulses  of,  57,  59. 

physiology  of,  51. 

pulsation  of,  141. 

white  matter  of,  26. 
Cerebral  cortex,  36,  41,  55. 
Cerebro-spinal  fluid,  105,  108,  137, 

139,  140. 
Cerebrum,  68. 

Cheyne-Stokes'  respiration,  106. 
Cholesteatoma,  76,  87. 
Cicatrices,  167. 
Clark,  59. 
Clarke's  column,  36. 
Climbing  fibers,  32,  33. 
Clivus,  23. 


183 


184 


INDEX 


Compensation,  71,  134. 
Conjugate  deviation,  107. 
Cord,  central  canal  of,  19. 
Corneal  anesthesia,  107. 
Corpora    quadrigemina,    posterior, 

21. 
Cortex  of  cerebellum,  26. 

cerebral,  30,  41,  55. 
Cranial   nerve   paralysis,   105,   107. 

nerves,  19. 
Crescentic  lobes,  anterior,  23. 

posterior,  23. 
Crossed  pyramidal  tracts,  44. 
Culmen,  2*1,  23. 
Cysts,  167. 

Death,  cause  of,  135,  147,  148. 
Decompression,  149. 
Deiters'  nucleus,  26,  30,  36,  41,  56. 
Deiterso-spinal  tract,  30. 
Delirium,  106. 
Dench,  146,  165. 
Dentate  nucleus,  26,  30. 
Deviations,  103,  114,  136,  139. 

conjugate,  107. 

spontaneous,  64,  65. 
Direction  centers,  61. 
Drainage  tubes,  159,  160,  161. 
Drowsiness,   106. 
Dura,  fistula  of,  141,  145. 
Dural  incision,  159, 

Ear,  internal,  17. 

Edingeu,  33,  59,  60. 

Electric  stimulation  of  cerebellum, 

59. 
Emaciation,  105,  108. 
Empyema,  saccus,  83. 
Encephaloscope,  160. 
Enduring  nystagmus,  69,  103,  133. 
Epidural  abscess,  82,  83,  140,  141, 

157. 
Epilepsy,  167. 
Equilibration,  53. 
Exploration  of  cerebellum  through 

occiput,   161,  162. 

Falling  reaction,  65,  103,  129,  139. 
Fasciculus,   posterior  longitudinal, 

30. 
Fibers  grimpantes,  32. 
Fifth  nerve,  root  of,  30,  40. 
Fillet,  mesial,  45. 
Fissures,  cerebellar,  21,  23. 
Fistula  of  dura,  141,  145. 


Flechsig's  tract,  33,  36,  56. 
Flocculi,  23. 
Focal  symptoms,  102. 
Folium  cacuminis,  23. 
Forced  movements,  52. 
Fossa,  posterior,  17. 
Fourth  ventricle,  19,  21,  26. 
Frenulum,  23. 

General  symptoms,  103. 
Gowers'  tract,  33,  37,  56. 
Granular  layer,  32. 
Granule  cells,  32. 

Head,  attitude  of,  103,  130. 
Headaches,  104,  105,  136,  141. 
Heimann,  146. 
Hemiparesis,  103,  130,  141. 

HORSLEY,    59. 

Hypermetria,  102,  109. 
Hypertony,  103,   113. 
Hysteria,  141. 

Incoordination,  53. 
Inferior  peduncles,  21. 
Internal  auditory  meatus,  19,  26. 
Internal  ear,  17. 

Joint,  55,  58,  60. 

Kernig's  sign,  140. 
Koch,  146. 
KOERNER,   146,  166. 
KoHNSTAaiM,  26,  30,  45. 
Krause,  160. 

Labyrinth,  static,  54,  55,  56,  58. 
Labyrinthectomy,  133,   139. 
Labyrinthitis,  157. 

suppurative,  74,  84. 
Lamina  of  cerebellum,  26. 
Latency  of  cerebellar  abscess,  134. 
Lateral  sinus,  17,  18,  26. 
Lewaxdowsky,  5-2,  53. 
Lingula,  21,  23. 
Lobes,  cerebellar,  21,  23. 
Lobus  centralis,  21,  23. 
Localizaton,  cerebellar,  61. 
Lotmar,  131. 
Lower  vermis,  20. 
Lumbar  puncture,  140. 

Maas,  131. 
Macewen,  146. 
Mastoid  antrum,  18. 


INDEX 


185 


Medulla,  17,  18,  20,  21. 
Meningitis,  139,  140. 

serous,   140. 

tuberculous,  140. 
^Mesial  fillet,  45. 

MlCHAELSEN,   157,   161. 

Mid-brain,   17,    18,  20. 

Middle  peduncles,  21. 

Molecular  layer,  32. 

Motor  impulses  of  cerebellum,  57, 

59. 
Muscles,  55,  56,  58,  60. 
Muscular  tonus,  58. 

Neck,  rigidity  of,  137. 
Neo-cerebellum,  59. 
Ner%'es,  cranial,  19. 
Neumann,  132,  133,  139,  146. 
Nodulus,  23. 
Nucleus  dentatus,  26,  30. 

emboliformis,  26,  30. 

globosus,  26,  30. 

motorius  tegmenti,  56. 

of  Goll  and  Burdach,  40. 

of  lateral  columns,  33. 

of  posterior  columns,  33. 

red,  36,  41. 

tecti,  26,  30. 

triangularis,  26,  30. 
Nystagmus,  103,  131,  132,  136,  138, 
157. 

Oculo-motor  nuclei,  45. 
Okada,  134. 
Olive,  upper,  40. 
Olivo-cerebellar  fibers,  36. 
Operation  in  two   stages,   149. 

methods  of  approach  in,  149,  150. 

through  sinus  walls,  165. 
Oppenheim,  146. 
Optic  nerve  changes,  105,  107,  140. 

Paleo-cerebellum,  59. 
Paracerebellar  nuclei,  26. 
Paralysis,  cranial  nerve,  105,  107. 
Peduncles,  20,  32,  33. 

inferior,  21. 

middle,  21. 
Petrous  pyramid,  17,  23. 
Physiology  of  cerebellum,  51. 
Pointing  reaction,  62. 
Pons,  17,  18,  20,  21,  30,  41. 

substantia  reticularis  of,  44. 

tegmentum   of,   41. 
Post-central  fissure,  21. 


Post-clival  fissure,  21. 
Post-nodular  fissure,  23. 
Post-pyramidal  fissure,  23. 
Posterior     corpora     quadrigemina, 
21. 

crescentic  lobes,  23. 

fossa,  17^ 

longitudinal  fasciculus,  30. 
Postero-inferior   lobes,   23. 
Postero-superior  lobes,  23. 
Precentral  fissure,  21. 
Preclival  fissure,  21. 
Prepyramidal  fissure,  23. 
Probst,  44. 

Prolapse  of  brain,  166,  167. 
Prophylactic  treatment,  148. 
Pulsation  of  cerebellum,  141. 
Purkinje   cells,  27,  32,  33. 
Pyramid,  23. 
Pyramidal  tracts,  crossed,  44. 

Reaction   movements,   64,   65,    103, 

129,  139. 
Recoveries  after  operation,   146. 
Red  nucleus,  36,  41. 
Reflexes,  105,  107,  140. 
Respiration,   disturbances   of,   105, 

106. 
Restiform  bodies,  21,  30. 
Rigidity  of  neck,  137. 
ROTHMANN,  59,  60. 
Rubro-spinal  tract,  36. 

Saccus  empyema,  83. 

Saccus  endolymphaticus,  19,  159. 

Sensitiveness  to  percussion,  137. 

Sensorium,    disturbances    of,    105, 
106. 

Sex  in  cerebellar  abscess,  77. 

Shimazono,  59. 

Sinus,  lateral,  17,  18,  26. 

Sinus  thrombosis,  79,  80,  84. 

Situation  of  cerebellar  abscess,  88. 

Skin,  55,  56,  58. 

Speech,  disturbances  of,   103,   113, 
136. 

Spinal  cord,  central   canal  of,   19. 

Spontaneous  cure  of  cerebellar  ab- 
scess, 145. 
deviation,  64,  65. 

Stages  of  cerebellar  abscess,  135. 

Static  labyrinth,  54,  55,  56,  58. 

Statotonus,  60. 

Substantia  rectlcularis  of  the  pons, 
44. 


186 


INDEX 


Superior  peduncles,  21. 
Suppurative  labyrinthitis,  79,  84. 
Sylvius,  acqueduct  of,  19. 

Tegmentum  of  pons,  41. 
Temperature  changes,  108. 
Tentorium  cerebelli,  17. 
Tonsils,  23. 

Tonus  centers  of  Barany,  67. 
Torcular  Herophili,  17. 
Tractus    Deiterso-spinalis,    36,    45, 
56. 

uncinatus,  36,  41,  56. 
Trautmann's  triangle,  158,  159,  160, 

162. 
Tremor,   103,  112. 
Uffenorde,  161. 
Upper  olive,  40. 

vermis,  20. 


U-shaped  dural  flap,  160. 
Uvula,  23. 

Ventral  cerebello-thalamic  bundle, 

36. 
Vermis,  19,  21,  23,  60. 

lesion  of,  65. 

lower,  20. 

upper,  20. 
Vertigo,  103,  133,  141. 
Vestibular  nerve,  30. 

nuclei,  26. 
Vomiting,  103,  104,  105,  133. 

Weight  estimation,  disturbances 
of,  103,  131. 

White  matter  of  cerebellum,  cen- 
tral,  26. 

Writing,  disturbances  of,  103,  112. 


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and  Packard In  Preparation. 

BRUCE:     Lectures  on  Tuberculosis  to  Nurses.     Based  on 
a   course   delivered   to   the   Queen  Victoria   Jubilee   Nurses. 
By  Olliver  Bruce,  m.r.c.s.,  l.r.c.p..  Joint  Tuberculosis  Officer, 
County  of  Essex. 
12mo,  Cloth,  124  Pages,  Illustrated $1.00  net. 

BRUNTON:     Therapeutics    op   the    Circulation,    By   Sir 
Lauder     Brunton,     m.d.,     d.sc,   ll.d.    Edin.,    ll.d.    Aberd., 
f.r.c.p.,   f.r.s.     Consulting  Physician  to  St.   Bartholomew's 
Hospital.     Second  Edition,  Entirely  Revised. 
Cloth,  xxiv-(-536  Pages,  110  Illustrations $2.50  net. 

BULKLEY:  Compendium  of  Diseases  of  the  Skin.  Based 
on  an  analysis  of  thirty  thousand  consecutive  cases.  With 
a  Therapeutic  Formulary,  by  L.  Duncan  Bulkley,  a.m., 
M.D.  Physician  to  the  New  York  Skin  and  Cancer  Hospital; 
Consulting  Physician  to  the  New  York  Hospital. 
8vo,  Cloth,  xviii+286  Pages $2.00  net. 

BULKLEY:     Cancer:     Its  Cause  and  Treatment.     By  L. 
Duncan  Bulkley. 
8vo,  Cloth,  224  Pages $1.50  net. 

BULKLEY:     Diet  and  Hygiene  in  Diseases  of  the  Skin. 
By  L.  Duncan  Bulkley. 
Svo,  Cloth,  xvi4-194  Pages $2.00  net. 

BULKLEY:  The  Influence  op  the  Menstrual  Function 
on  Certain  Diseases  op  the  Skin.  By  L.  Duncan  Bulkley. 
12mo,  Cloth,  108  Pages $1.50  net. 

BULKLEY:     The  Relations  op  Diseases  of  the  Skin  to 
Internal  Disorders  :  With  Observations  on  Diet,  Hygiene 
AND  General  Therapeutics.     By  L.  Duncan  Bulkley. 
12mo,  Cloth,  175  Pages $1.50  net. 

BULKLEY:  Pb*nciples  and  Application  of  Local  Treat- 
ment IN  Diseases  op  the  Skin.  By  L.  Duncan  Bulkley. 
12mo,  Cloth,  130  Pages $1.50  net. 


HOEBEB'S  MEDICAL  MONOGBAPHS  3 

CAUTLEY:     The  Diseases  op  Infants  and  Children.     By- 
Edmund  Cautley,  m.d.  Cantab.,  f.r.c.p.  Lond.     Senior  Physi- 
cian  to   the  Belgrave   Hospital  for  Children;    Physician   to 
the  Metropolitan  Hospital;   etc. 
Large  8vo,  Cloth,  1042  Pages $7.00  net. 

CLARKE :  Problems  in  the  Accommodation  and  Refraction 
OF  THE  Eye,  a  Brief  Review  of  the  Work  of  Bonders, 
and  THE  Progress  Made  During  the  Last  Fifty  Years.  By 
Ernest  Clarke,  m.d.,  b.s.,  f.r.c.s.  Senior  Surgeon  to  the 
Central  London  Ophthalmic  Hospital,  Consulting  Ophthalmic 
Surgeon  to  the  Miller  General  Hospital. 
8vo,  Boards,  110  Pages $1.00  net. 

COOKE:  The  Position  of  the  X-Rays  in  the  Diagnosis 
AND  Prognosis  of  Pulmonary  Tuberculosis.  By  W.  E. 
Cooke,  M.B.,  m.r.c.p.e.,  d.p.h.  (Lond.),  Medical  Superin- 
tendent, Ochil  Hills  Sanatorium  and  Coppins  Green  Industrial 
Sanatorium.     8vo,  Cloth,  Illustrated. $1.50  net. 

COOPER:  Pathological  Inebriety.  Its  Causation  and 
Treatment.  By  J.  W.  Astley  Cooper.  Medical  Superin- 
tendent and  Licensee  of  Ghyllwood  Sanatorium  near  Cocker- 
mouth,  Cumberland.  With  Introduction  by  Sir  David  Fer- 
rier,  m.d.,  f.r.s.    12mo,  Cloth,  xvi+151  Pages $1.50  net. 

COOPER:     The   Sexual   Disabilities   of   Man,   and    Their 
Treatment.    By  Arthur  Cooper.     Consulting  Surgeon  to  the 
Westminster  General  Dispensary;    Formerly  Surgeon  to  the 
Male  Lock  Hospital,  London. 
2nd  Edition,  12mo,  Cloth,  viii-(-204  Pages $2.00  net. 

CORBETT-SMITH :  The  Problem  of  the  Nations,  A  Study 
in  the  Causes,  Symptoms  and  Effects  of  Sexual  Disease,  and 
the  Education  of  the  Individual  Therein.  By  A.  Corbett- 
Smith,  Editor  of  The  Journal  of  State  Medicine;  Lec- 
turer in  Public  Health  Law  at  the  Royal  Institute  of  Public 
Health.    Large  Svo,  Cloth,  xii+107  Pages $1.00  net. 

CORNET:     Acute  General  Miliary  Tuberculosis.    By  Pro- 
fessor Dr.   G.   Cornet,   Berlin  and  ReichenhaU.     Translated 
by  F.  S.  Tinker,  b.a.,  m.b.,  etc. 
Svo,  Cloth,  viii+lO?  Pages $1.50  net. 

CEOOKSHANK:     Flatulence  and  Shock.    By  F.  G.  Crook- 
shank,  m.d.  Lond.,  M.R.c.p.    Physician  (Out  Patients)  Hamp- 
stead  General  and  N.  W.  Lond.  Hospital ;  Assistant  Physician 
The  Belgrave  Hospital  for  Children  S.  W. 
Svo,  Cloth,  iv+47  Pages $1.00  net. 

DAVIDSON:  Localization  by  X-Eays  and  Steeboscopt. 
By  Sir  James  Mackenzie  Davidson,  m.b,,  cm.  Aberd.  Con- 
Bulting   Medical   OflSicer,   Roentgen  Eay   Department,   EoyaJ 


4  HOEBEB'S  MEDICAL  MONOGEAPHS 

London  Ophthalmic  Hospital,  and  X-Ray  Department,  Char- 
ing Cross  Hospital;  Fellow,  Physical  Society;  President, 
Radiology  Section,  Seventeenth  International  Congress  of 
Medicine.  8vo,  Cloth,  72  Pages,  Plates  and  58  Stereoscopic 
Figures    $3.00  net. 

DELORME:  War  Surgery.  By  Edmond  Delorme,  General 
Medical  Inspector  of  the  French  Army.  Translated  by  D. 
De  Merie,  Surgeon  to  In-Patients,  French  Hospital,  London. 
12mo,  Cloth,  Illustrated,  248  Pages $1.50  net. 

EDRIDGE-GREEN:  The  Hunterian  Lectures  on  Colour- 
Vision  AND  Colour  Blindness.  Delivered  before  the  Royal 
College  of  Surgeons  of  England  on  February  1st  and  3rd, 
1911.  By  Professor  F.  W.  Edridge-Green,  m.d.  Durh., 
F.R.c.s.  England.  Beit  Medical  Research  Fellow. 
8vo,  Cloth,  x-l-76  Pages $1,50  net. 

EHRLICH:  Experimental  Researches  on  Specific  Thera- 
peutics. By  Prof.  Paul  Ehrlich,  m.d.,  d.sc.  Oxon.  Director 
of  the  Konigliches  Institut  fiir  Experimentelle  Therapie, 
Frankfort.  The  Harben  Lectures  for  1907  of  The  Royal 
Institute  of  Public  Health. 
16mo,  Cloth,  x+95  Pages $1.00  net. 

EINHORN:      Lectures    on    Dietetics.      By    Max    Einhorn, 
Professor  of  Medicine  at  the  New  York  Post-Graduate  Med- 
ical   School    and    Hospital    and    Visiting    Physician    to    the 
German  Hospital,  New  York. 
12mo,  Cloth,  xvi-[-156  Pages $1.00  net. 

ELLIOT :     Sclero-Corneal     Trephining  in  the  Operative 
Treatment  of  Glaucoma.     By  Robert  Henry  Elliot,  m.d., 
B.s.    Lond.,   d.sc.    Edin.,   f.r.c.s.   Eng.,   etc.     Lieut.    Colonel 
i.m.s.     Second   Edition. 
8vo,  Cloth,  135  Pages,  33  Illustrations $3.00  net. 

EMERY :  Immunity  and  Specific  Therapy.  By  Wm,  D  'Este 
Emery,  m.d.,  b.sc.  Lond.  Clinical  Pathologist  to  King's 
College  Hospital  and  Pathologist  to  the  Children's  Hospital, 
Paddington  Green;  formerly  Assistant  Bacteriologist  to  the 
Royal  College  of  Physicians  and  Surgeons,  and  some  time 
Lecturer  on  Pathology  and  Bacteriology  in  the  University 
of  Birmingham. 

Svo,  Cloth,  448  Pages,  with  2  Illustrations $3.50  net. 

adopted  by  the  u.  s.  army. 

FRIESNER  AND  BRAUN:  Cerebellar  Abscess;  Its  Eti- 
ology, Pathology,  Diagnosis  and  Treatment.  By  Isidore 
Friesner,  m.d.,  f.a.c.s..  Adjunct  Professor  of  Otology  and 
Assistant  Aural  Surgeon,  Manhattan  Eye,  Ear  and  Throat 
Hospital  and  Post,  Graduate  Medical  School,  and  Alfred 
Braun,   m.d.,   f.a.c.s.,   Assistant  Aural  Surgeon,   Manhattan 


HOEBEE'S  MEDICAL  MONOGBAPHS  5 

Eye,  Ear  and  Throat  Hospital,  Adjunct  Professor  of 
Laryngology,  New  York  Polyclinic  Hospital  and  Medical 
School  and  Adjunct  Otologist,  Mt.  Sinai  Hospital.  8vo,  Cloth, 
about  200  Pages,  10  Plates,  16  Illustrations $2.50  net. 

GHON:     The    Phimaby    Lung    Focus    of    Tuberculosis    in 
Children.     By  Anton   Ghon,   m.d.,   English   Translation  by 
D.  Barty  King,  m.a.,  m.d.  Edin.,  m.r.c.p..  Assistant  Physician 
to  the  Eoyal  Hospital  for  Diseases  of  the  Chest. 
196  Pages,  72  Text  Figures  and  2  Plates $3.75  net. 

GILES:  Anatomy  and  Physiology  op  the  Female  Genera- 
tive Organs  and  of  Pregnancy.  By  Arthur  E.  Giles,  m.d., 
B.sc.  Lond.,  M.R.C.P.  Lond.;  F.R.c.s.  Ed.  Gynecologist  to  the 
Prince  of  Wales  General  Hospital,  Tottenham,  and  Surgeon 
to  the  Chelsea  Hospital  for  Women. 
Large  8vo,  24  Pages,  with  Mannikin $1.50  net. 

GOULSTON:  Cane  Sugar  and  Heart  Disease.  By  Arthur 
Goulston,  M.A.,  m.d.  Cantab.  Hunterian  Society's  Medallist, 
1912.     8vo,  Cloth,  107  Pages $2.00  net. 

GEEEFF:  Guide  to  the  Miceoscopic  Examination  of  the 
Eye.  By  Professor  E.  Greeff.  Director  of  the  University 
Ophthalmic  Clinique  in  the  Eoyal  Charity  Hospital,  Berlin. 
With  the  co-operation  of  Professor  Stock  and  Professor 
Wintersteiner.  Translated  from  the  third  German  Edition 
by  Hugh  Walker,  m.d.,  m.b.,  cm.  Ophthalmic  Surgeon  to 
the  Victoria  Infirmary,  Glasgow. 
Large  8vo,  Cloth,  86  Pages,  Illustrated $2.00  net. 

HAEEIS:  Lectures  on  Medical  Electricity  to  Nurses. 
An  Illustrated  Manual  by  J.  Delpratt  Harris,  m.d.  Durh., 
M.R.c.s.  Senior  Surgeon  and  Honorary  Medical  OflSeer  in 
charge  of  the  Electrical  Department,  Eoyal  Devon  Hosp. 
12mo,  Cloth,  88  Pages,  Illustrated $1.00  net. 

HELLMAN:  Amnesia  and  Analgesia  in  Parturition — 
Tvs^iLiGHT  Sleep.  By  Alfred  M.  Hellman,  b.a.,  m.d.,  f.a.c.s. 
8vo,  Cloth,  with  Charts,  200  Pages $1.50  net. 

HEWATT:  The  Examination  of  the  Urine,  and  Other 
Clinical  Side  Eoom  Methods.     By  Andrew  Fergus  Hewatt, 

M.B.,    CH.B.,    M.R.C.P.    Edin. 

16mo,  5th  Edition,  Numerous  Illustrations $  .75  net. 

HOFMANN-GAESON :  Eemedial  Gymnastics  fob  Heart 
Affections.  Used  at  Bad-Nauheim.  Being  a  Translation 
of  "Die  Gymnastik  der  Herzleidenden "  von  I)r.  Med.  Julius 
Hofmann  und  Dr.  Med.  Ludwig  Pohlman.  Berlin  and  Bad- 
Nauheim.  By  John  George  Garson,  m.d.  Edin.,  etc.  Physi- 
cian to  the  Sanatoria  and  Bad-Nauheim,  Eversley,  Hants. 
With  51  Full-page  Illustrations  and  Diagrams.  Large  8vo, 
Cloth,  xvi+128  Pages $2.00  net. 


6  HOEBER'S  MEDICAL  MONOGEAPHS 

HOWAKD:     The  Therapeutic  Value  op  the  Potato.     By 
Heaton  C.  Howard,  l.e.c.p.  Lond.,  m.b.c.s.  Eng. 
8vo,  Paper,   vi+31   Pages,   Illustrated 50c 

JELLETT:  A  Short  Practice  op  Midwifery  for  Nurses. 
Embodying  the  treatment  adopted  in  the  Rotunda  Hospital, 
Dublin.  By  Henry  Jellett,  b.a.,  m.d.  (Dublin  University), 
P.R.C.P.I.,  Master  Rotunda  Hospital;  Extern  Examiner  in 
Midwifery  and  Gynecology,  Victoria  University,  Manchester; 
Late  King's  Professor  of  Midwifery;  University  of  Dublin. 
With  Six  Plates  and  169  Illustrations  in  the  Text,  also 
an  Appendix,  a  Glossary  of  Medical  Terms,  and  the  Regu- 
lations of  the  Central  Midwives  Board. 
12mo,  Cloth,  xvi-)-508  Pages $2.50  net. 

KENWOOD :  Public  Health  Laboratory  Work.  By  Henry 
R.  Kenwood,  m.b.,  f.r.s.  Edin.,  p.p.h.,  f.c.s.,  Chadwick. 
Professor  of  Hygiene  and  Public  Health,  University  of  Lon- 
don; Medical  Officer  of  Health  and  Public  Analyst  for  the 
Metropolitan  Borough  of  Stoke  Newington;  Examiner  in 
Public  Health  to  the  Royal  College  of  Physicians  and 
Surgeons,  London,  etc. 
6th  Edition,  8vo,  Cloth,  418  Pages,  Illustrated $4.00  net. 

KERLEY:     What  Every  Mother  Should  Know  About  Her 
Infants  and  Young  Children.    By  Charles  Gilmore  Kerley, 
M.D.     Professor  of  Diseases  of   Children,  N.   Y.   Polyclinic 
Medical    School    and    Hospital. 
Svo,  Paper,  107  Pages 35c  net. 

KETTLE:  The  Pathology  op  Tumors.  By  E.  H.  Kettle, 
M.D.,  B.S.,  Assistant  Pathologist,  St.  Mary's  Hospital,  and 
Assistant  Lecturer  on  Pathology,  St.  Mary's  Hospital  Med- 
ical School.    About  240  Pages,  126  Illustrations. .  .$3.00  net. 

LEWERS:  A  Practical  Textbook  op  the  Diseases  op 
Women.  By  Arthur  H.  N.  Lewers,  m.d.  Lond.  Senior 
Obstetric  Physician  to  the  London  Hospital;  Late  Examiner 
in  Obstetric  Medicine  at  the  University  of  London;  Univer- 
sity Scholar  &  Gold  Medallist  in  Obstetric  Medicine,  London 
University,  etc. 

With  258  Illustrations,  13  Colored  Plates,  5  Plates  in  Black 
and  White.    7th  Edition,  8vo,  Cloth,  xii+540  Pages. $4.00  net. 

LEWIS :  Clinical  Disorders  of  the  Heart  Beat.  A  Hand- 
book for  Practitioners  and  Students.  By  Thomas  Lewis,  m.d,, 
D.sc,  F.R.c.p.  Assistant  Physician  and  Lecturer  in  Cardiac 
Pathology,  University  College  Hospital  Medical  School, 
Physician  to  Out-Patients,  City  of  London  Hospital  for 
Diseases  of  the  Chest. 
3rd  Ed.,  Svo,  Cloth,  116  Pages,  54  Illustrations.  .$2.00  net. 


EOEBEB'S  MEDICAL  MONOGBAPHS  7 

LEWIS:     Lectures  on  the  Heart.     Comprising  the  Herter 
Lectures   (Baltimore),  a  Harvey  Lecture   (New  York),  and 
an  Address  to  the  Faculty  of  Medicine  at  McGill  University 
(Montreal).     By  Thomas  Lewis. 
124  Pages,  with  83  Illustrations $2.00  net. 

LEWIS :  Clinical  Electrocardiography.  By  Thomas  Lewis. 
8vo,  Cloth,   120   Pages,  with  Charts $2.00  net. 

LEWIS :  The  Mechanism  of  the  Heart  Beat.  With  Special 
Keference  to  Its  Clinical  Pathology.  By  Thomas  Lewis. 
Large  Svo,  Cloth,  295  Pages,  227  lUus $7.00  net. 

McCLUEE:  A  Handbook  of  Fevers.  By  J.  Campbell  Mc- 
Clure,  M.D.,  Glasgow.  Physician  to  Out-Patients,  The 
French  Hospital,  and  Physician  to  the  Margaret  Street 
Hospital  for  Consumption  and  Diseases  of  the  Chest,  London. 
Svo,  Cloth,  470  Pages,  with  Charts $3.50  net. 

McCRUDDEN:    The  Chemistry,  Physiology  and  Pathology 
of  Uric  Acid,  and  the  Physiologically  Important  Purin 
Bodies.    With  a  Discussion  of  the  Metabolism  in  Gout.    By 
Francis   H.    MeCrudden. 
12mo,  Paper,  318  Pages $2.00  net. 

McKISACK:    Systematic   Case  Taking.     A  Practical  Guide 
to  the  Examination  and  Recording  of  Medical  Cases.     By 
Henry  Lawrence  McKisack,  m.d.,  m.r.c.p.  Lond.     Physician 
to  the  Royal  Victoria  Hospital,  Belfast. 
12mo,  Cloth,  166  Pages $1.50  net. 

MACKENZIE:     Symptoms  and  Their  Interpretations.    By 
James  Mackenzie,  m.d.,  ll.d.  Aber.  and  Edin.     Lecturer  on 
Cardiac  Research,   London   Hospital. 
Svo,  Cloth,  Illustrated,  xxii4-304  Pages $3.00  net. 

MACMICHAEL :  The  Gold-Headed  Cane.  By  William  Mac- 
michael.  Reprinted  from  the  2nd  Edition.  With  a  Preface 
by  Sir  William  Osier  and  an  Introduction  by  Dr.  Francis  E. 
Packard.  Printed  from  large  Scotch  type  on  a  special  heavy- 
weight paper,  5%  by  7%  inches,  bound  in  blue  Italian  hand- 
made paper,  with  parchment  back,  gilt  top,  square  back, 
and  gold  stamping  on  back  and  side $3.00  net. 

MAGILL:     Notes  on  Galvanism  and  Faradism.     By  E.  M. 
Magill,  M.B.,  B.s.  Lond.,  R.c.s.i.   (Hons.) 
12mo,  Cloth,   220  Pages,  67  Illustrations $1.50  net. 

MARTINDALE    and    WESTCOTT:     "Salvarsan"    "606" 
(Dioxy-Diamino-Arsenobenzol),  Its  Chemistry,  Pharmacy 
AND  Therapeutics.    By  W.  Harrison  Martindale,  ph.d.  Mar- 
burg,  F.C.S.,  and  W.  Wynn  Westcott,  m.b. 
Svo,  Cloth,  xvi-l-76  Pages $1.50  net. 


ff  HOEBEB'S  MEDICAL  MONOGBAPHS 

MINETT:     Diagnosis  of  Bacteria  and  Blood  Parasites.    By 

E.  P.  Minett,  M.D.,  d.p.h.,  d.t.m.  and  H.,  m.r.c.s.,  l.r.c.p. 
Assistant  Government  Medical  OflBcer  of  Health  and  Bacteri- 
ologist British  Guiana. 

12mo,  Cloth,  viii+80  Pages $1.00  net. 

MOTT :    Nature  and  Nurture  in  Mental  De\':elopment.    B7 

F.  W.  Mott,  M.D.,  F.R.S.,  F.R.c.P.     Pathologist  to  the  London 
County    Asylums,    Consulting    Physician    to    Charing    Cross 
Hospital  and  the  Queen  Alexandra  Military  Hospital. 
12mo,   Cloth,   151    Pages,   with   Diagrams $1.50   net. 

MUERELL:     What  To  Do  in  Cases  or  Poisokino.    By  Wil- 

Uam  Murrell,  m.d.,  f.r.c.p.  Senior  Physician  to  the  West- 
minster Hospital;  Lecturer  on  Clinical  Medicine  and  Joint 
Lecturer  on  the  Principles  and  Practice  of  Medicine;  Late 
Examiner  in  the  Universities  of  Edinburgh,  Glasgow  and 
Aberdeen,  and  to  the  Royal  College  of  Physicians. 
11th  Edition,  16mo,  Cloth,  283  Pages $1.00  net. 

OLIVER :  Lead  Poisoning  :  From  the  Industrial,  Medical 
AND  Social  Point  of  View.  Lectures  Delivered  at  the  Royal 
Institute  of  Public  Health.  By  Sir  Thomas  Oliver,  m.a.,  m.d., 
P.R.C.P.  Consulting  Physician,  Royal  Victoria  Infirmary,  and 
Professor  of  the  Principles  and  Practice  of  Medicine,  Uni- 
versity of  Durham  College  of  Medicine,  Newcastle-upon-Tyne, 
Late  Medical  Expert,  Dangerous  Trades  Committee;  Home 
Office.     Large  12mo,  Cloth,  294  Pages $2.00  net. 

OSLER:  Tv?o  Essays.  By  Sir  William  Osier,  m.d.  Regius 
Professor  of  Medicine  at  Oxford. 

Vol.  1.  A  Way  of  Life.  An  Address  to  Yale  Students, 
Sunday  Evening,  April  20th,  1913.  16mo,  Cloth,  61 
Pages 50c  net. 

Vol.  2.  Man's  Redemption  of  Man.  A  Lay  Sermon, 
McEwan   Hall,   Edinburgh,   Sunday,   July   2d,    1910.      16mo, 

Cloth,  63  Pages 50c  net. 

The  Set  Neatly  Bound  and  Boxed $1.00  net. 

(A  handsome  presentation  set.) 

OTT:  Fever,  Its  Thermotaxis  and  Metabolism.  By  Isaac 
Ott,  a.m.,  m.b.  Professor  of  Physiology  in  the  Medico- 
Chirurgical  College  of  Philadelphia;  Ex-Fellow  in  Biology 
Johns  Hopkins  University;  Consulting  Neurologist,  Norris- 
tovm  Asylum,  Penna. ;  Ex-President  of  American  Neuro- 
logical Association,  etc. 
12mo,  Cloth,  168  Pages,  Illustrated $1.50  net. 

PAGET :  For  and  Against  Experiments  on  Animals.  Evi- 
dence before  the  Royal  Commission  of  Vivisection.  By 
Stephen  Paget,  f.e.c.s.     Hon.   Secretary  Research  Defence 


EOEBEE'S  MEDICAL  HON OGR APES  » 

Society.    With  an  Introduction  by  The  Eight  Hon.  The  Earl 

of  Cromer,  o.M.,  g.c.m.g.,  g.c.b. 

8vo,  Cloth,  Illustrated,  xii-|-344  Pages $1.50  net. 

PEGLER:  Map  Scheme  op  the  Sensory  Distribution  of 
THE  Fifth  Nerve  (Trigeminus)  with  Its  Ganglia  and 
Connections.  By  L.  Hemington  Pegler,  m.d,,  m.b,c.s.  Senior 
Surgeon,  Metropolitan  Ear,  Nose  and  Throat  Hospital,  etc. 

Mounted  on  Eollers,  4ft.  1  in.  x.  4  ft.  8  in $7.00  net. 

Folded  in  Cloth   Binder $8.00  net. 

RAWLING:  Landmarks  and  Surface  Markings  of  the 
Human  Body.  By  L.  Bathe  Rawling,  m.b.,  b.c.  (Cant.), 
F.R.c.s.  (Lond.)  Surgeon  with  Charge  of  Out-Patients,  Late 
Senior  Demonstrator  of  Anatomy  at  St.  Bartholomew's  Hos- 
pital; Late  Assistant-Surgeon  to  the  German  Hospital, 
Dalston;  Late  Hunterian  Professor  Royal  College  of 
Surgeons,  England,  etc. 
5th  Ed.,  8vo,  Cloth,  31  Plates,  xii-fQe  Pages  of  Text.  $2.00  net. 

RITCHIE :  Auricular  Flutter.  By  William  Thomas  Ritchie, 
M.D.,  F.R.C.P.E.,  f.r.s.e.  Physician  to  the  Royal  Infirmary; 
Lecturer  on  the  Practice  of  Medicine,  School  of  Medicine 
of  the  Royal  Colleges;  Lecturer  on  Clinical  Medicine  in  the 
University  of  Edinburgh.  Large  8vo,  Cloth,  xii+144  Pages, 
21  Plates,  107  Illustrations $3.50  net. 

VON    RUCK    and    von    RUCK:     Studies    in    Immunization 
against    TuBERCtJi.osis.      By    Karl    von    Ruck,    m.d.,    and 
Silvio  von  Ruck,  m.d. 
8vo,  Cloth,  about  440  Pages $3.50  net. 

RUTHERFORD :  The  Ileo-C^cal  Valve.  By  A.  H.  Ruther- 
ford, M.D.  Edin.  8vo,  Cloth,  63  Pages  of  Text,  23  Full  Page 
Plates,  3  of  Which  Are  Colored $2.25  net. 

SAALFELD  :  Lectures  on  Cosmetic  Treatment.  A  Manual 
for  Practitioners.  By  Dr.  Edmund  Saalfeld  of  Berlin. 
Translated  by  J.  F.  Dally,  m.a.,  m.d.,  b.c.  Cantab., 
M.B.c.p.  Lond.  Physician  to  the  St  Marylebone  General 
Dispensary.  With  an  Introduction  and  Notes  by  P.  S.  Abra- 
ham, M.A.,  M.D.,  B.sc,  F.R.C.S.I.,  Surgeon  for,  and  Lecturer 
on.  Diseases  of  the  Skin,  West  London  Hospital  and  College. 
Late  Surgeon  to  the  Skin  Hospital,  Blackfriars. 
12mo,  Cloth,  xii+186  Pages,  Illustrated $1.75  net. 

SCHOOL  OF  SALERNO,  THE:  New  Edition,  Edited  by 
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SCOTT :  Modern  Medicine  and  Some  Modern  Remedies.  By 
Thomas  Bodley  Scott,  with  a  Preface  by  Sir  Lauder  Brunton. 
8vo $1.50  nt!t. 


10  HOEBEE'S  MEDICAL  MONOGBAPHS 

SCOTT:    The  Eoad  to  a  Healthy  Old  Age.     Essays  by 
Thomas  Bodley  Scott,  m.d. 
12mo,  Cloth,  104  Pages $1.00  net. 

SENATOR  and  KAMINER:  Maeriage  and  Disease.  Being 
an  Abridged  Edition  of  "Health  and  Disease  in  Relation  to 
Marriage  and  the  Married  State. ' '  By  Professor  H.  Senator 
and  Dr.  S.  Kaminer.  Translated  from  the  German  by  J. 
Dulberg,  m.d. 
8vo,  Cloth,  452  Pages $2.50  net. 

SMITH:  Some  Common  Remedies,  and  Their  Use  in  Prac- 
tice. By  Eustace  Smith,  m.d.  Fellow  of  the  Royal  CoUege 
of  Physicians;  Senior  Physician  to  the  East  London  Hospital 
for  Children;  Consulting  Physician  to  the  Victoria  Park 
Hospital  for  Diseases  of  the  Chest. 
8vo,  Cloth,  viii4-112  Pages $1.25  net. 

SQUIER   and   BUGBEE:     Manual   of  Cystoscopy.     By   J. 
Bently  Squier,  m.d.     Professor  of   Genito-Urinary  Surgery, 
New  York  Post-Graduate  Medical  School  and  Hospital,  and 
Henry  G.  Bugbee,  m.d. 
8vo,  Flex.  Leather,  xiv+117  Pages,  26  Colored  Plates  $3.00  net. 

ADOPTED   BY   THE   U.    S.   ARMY. 

STARK:  The  Growth  and  Development  of  the  Baby,  A 
tabular  chart,  giving  the  result  of  personal  observation,  veri- 
fied by  authoritative  data,  as  to  development,  weight,  height, 
etc.,  during  the  first  seven  years.  By  Morris  Stark,  m.a.,  b.s., 
M.D.  Instructor  of  Pediatrics,  New  York  Post-Graduate 
Medical  School,  etc. 
Heavy  Paper,  20  by  25  inches 50c  net. 

STEPHENSON:     Eye-Strain  in  Eveey-day  Practice.     By 
Sidney  Stephenson,  M.B.,  CM.  Edin.,  D.o.  Oxon.,  f.r.c.s.  Edin. 
Ophthalmic  Surgeon  to  the  Queen's  Hospital  for  Children; 
Editor  of  the  Ophthalmoscope. 
Svo,  Cloth,  x-fl39  Pages $1.50  net. 

STEPHENSON:     A  Review  of  Hormone  Therapy.     1913. 

Svo,  Cloth,  viii+170  Pages $1.00  net. 

Bound    and   interleaved   edition   of   the   famous   "Hormone 
Number"  of  the  Prescriber   (Edinburgh). 

SWIETOCHOWSKI:      Mechano-Therapeutics    in    General 
Practice.    By  G.  de  Swietochowski,  m.d.,  m.r.c.s.    FeUow  of 
the  Royal  Society  of  Medicine;  Clinical  Assistant,  Electrical 
and  Massage  Department,  King's  College  Hosp. 
12mo,  Cloth,  xiv-f  141  Pages,  31  Illustrations $1.50  net. 

TOUSEY:  Roentgen ographic  Diagnosis  op  Dental  Infec- 
tion in  Systemic  Diseases.  By  Sinclair  Tousey,  a.m.,  m.d. 
About  72  Pages  and  70  Illustrations $1.50  net. 


HOEBER'S  MEDICAL  MONOGBAPHS  11 

TUENER  and  PORTER:  The  Skiagraphy  of  the  Acces- 
sory Nasal  Sinuses.  By  A.  Logan  Turner,  m.d.,  f.r.c.s.e., 
F.R.s.E.  Surgeon  to  the  Ear  and  Throat  Department,  the 
Royal  Infirmary,  Edinburgh,  and  W.  G.  Porter,  m.b,,  b.sc, 
F.R.C.S.E.  Surgeon  to  Eye  and  Throat  Infirmary,  Edinburgh. 
Quarto,  Cloth,  45  Pages  of  Text,  39  Plates $4.50  net. 

WANKLYN:  How  to  Diagnose  Smallpox.  A  Guide  for 
General  Practitioners,  Post-Graduate  Students,  and  Others. 
By  W.  McC.  Wanklyn,  b.a.  Cantab.,  m.r.c.s.,  l.r.c.p.,  d.p.h. 
Assistant  Medical  Ofiicer  of  the  London  County  Council  and 
formerly  Medical  Superintendent  of  the  River  Ambulance 
Service  (Small-pox). 
8vo,  Cloth,  102  Pages,  Illustrated $1.50  net. 

WATSON:  Gonorrhcea  and  Its  Complications  in  the  Male 
AND  Female.  By  David  Watson,  m.b.,  cm.,  Surgeon,  Glasgow 
Lock  Hospital  Dispensary,  Surgeon  for  Venereal  Diseases, 
Glasgow  Royal  Infirmary,  etc.,  etc.  8vo,  Cloth,  375  Pages, 
72  Illustrations,  12  Plates,  Some  Colored $3.75  net. 

WHITE :     The  Pathology  of  Growth.  Tumours.  By  Charles 
Powell    White,    M.c,    f.r.c.s.      Director,    Pilkington    Cancer 
Research  Fund,  Pathologist  Christie  Hospital,  Special  Lec- 
turer in  Pathology,  University  of  Manchester. 
8vo,  Cloth,  xvi-(-235  Pages,  Illustrated $3.50  net. 

WHITE:  Occupational  Affections  of  the  Skin.  A  brief 
account  of  the  trade  Processes  and  Agents  which  give  rise 
to  them.  By  P.  Prosser  White,  m.d.,  Ed.,  m.r.c.s.  Lond.  Life 
Vice-President,  Senior  Physician  and  Dermatologist,  Royal 
Albert  Edward  Infirmary,  Wigan,  Vice-President,  Assoc. 
Certif.  Fact.  Surgeon;  Life  Fellow,  Lond.  Dermat.  Society. 
8vo,  Cloth,  165  Pages $2.00  net. 

WICKHAM  and  DEGRAIS:  Radium.  As  employed  in  the 
treatment  of  Cancer,  Angiomata,  Keloids,  Local  Tuberculosis 
and  other  affections.  By  Louis  Wickham,  m.v.o.  Medecin 
de  St.  Lazare;  Ex-Chef  de  Clinique  a  L'Hopital  St. 
Louis,  and  Paul  Degrais,  Ex-Chef  de  Laboratoire  k  L  'Hopital 
St.  Louis.  Chefs  de  service  au  Laboratoire  Biologique  du 
Radium;  Laureats  de  L 'Academic  de  Medecine. 
8vo,  Cloth,  53  Illustrations,  viii-[-lll  Pages $1.25  net. 

WRENCH :     The  Healthy  Marriage.    A  Medical  and  Psycho- 
logical Guide  for  Wives.    By  G.  T.  Wrench,  m.d.,  b.s.  Lond., 
Past  Assistant  Master  of  the  Rotunda  Hospital,  Dublin. 
8vo,   Cloth,   x-f300   Pages $1.50  net. 

WEIGHT:     The  Unexpurgated  Case  against  Woman  Suf- 
frage.    By  Sir  Almroth  E.  Wright,  m.d.,  f.r.s. 
Svo,  Cloth,  xii-|-188  Pages $1.00  net. 


12  EOEBER'S  MEDICAL  MONOGBAPHS 

WEIGHT:  On  Phaemaco-Therapy  and  Preventive  Inocu- 
lation ;  Applied  to  Pneumonia  in  the  African  Native,  with 
a  Discourse  on  the  Logical  Methods  Which  Ought  to  Be 
Employed  in  the  Evaluation  of  Therapeutic  Agents.  B7 
Sir  Almroth  E.  Wright,  m.d.,  f.r.s. 
8vo,  Cloth,  124  Pages $2.00  net. 

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